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Archive for the ‘Neuropathy’ Category

Diabetic Neuropathy Drugs Market Size By Product Analysis, Application, End-Users, Regional Outlook, Competitive Strategies And Forecast Up To 2026 -…

Sunday, July 12th, 2020

New Jersey, United States,- Latest update on Diabetic Neuropathy Drugs Market Analysis report published with extensive market research, Diabetic Neuropathy Drugs Market growth analysis, and forecast by 2026. this report is highly predictive as it holds the overall market analysis of topmost companies into the Diabetic Neuropathy Drugs industry. With the classified Diabetic Neuropathy Drugs market research based on various growing regions, this report provides leading players portfolio along with sales, growth, market share, and so on.

The research report of the Diabetic Neuropathy Drugs market is predicted to accrue a significant remuneration portfolio by the end of the predicted time period. It includes parameters with respect to the Diabetic Neuropathy Drugs market dynamics incorporating varied driving forces affecting the commercialization graph of this business vertical and risks prevailing in the sphere. In addition, it also speaks about the Diabetic Neuropathy Drugs Market growth opportunities in the industry.

Diabetic Neuropathy Drugs Market Report covers the manufacturers data, including shipment, price, revenue, gross profit, interview record, business distribution etc., these data help the consumer know about the competitors better. This report also covers all the regions and countries of the world, which shows a regional development status, including Diabetic Neuropathy Drugs market size, volume and value, as well as price data.

Diabetic Neuropathy Drugs Market competition by top Manufacturers:

Diabetic Neuropathy Drugs Market Classification by Types:

Diabetic Neuropathy Drugs Market Size by End-user Application:

Listing a few pointers from the report:

The objective of the Diabetic Neuropathy Drugs Market Report:

Cataloging the competitive terrain of the Diabetic Neuropathy Drugs market:

Unveiling the geographical penetration of the Diabetic Neuropathy Drugs market:

The report of the Diabetic Neuropathy Drugs market is an in-depth analysis of the business vertical projected to record a commendable annual growth rate over the estimated time period. It also comprises of a precise evaluation of the dynamics related to this marketplace. The purpose of the Diabetic Neuropathy Drugs Market report is to provide important information related to the industry deliverables such as market size, valuation forecast, sales volume, etc.

Major Highlights from Table of contents are listed below for quick lookup into Diabetic Neuropathy Drugs Market report

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KEEPING THE FAITH | Even when it’s hard, love your enemies – Mahoning Matters

Sunday, July 12th, 2020

We are afforded opportunities daily to be gracious and merciful. It is a superpower to be embraced: the ability to treat someone who offended you with compassion; choosing to be kind and forgiving.

Matthew 5:9, the Messiah declares, Blessed are the peacemakers, for they shall be called the sons of God.

Yet, how does this impact the exchange when the store clerk gives you a hard time with a return; when that car in front of you turns abruptly without signaling; or when a friend betrays your confidence and shares your personal matters with others.

We are afforded opportunities daily to be gracious and merciful. It is a superpower to be embraced: the ability to treat someone who offended you with compassion; choosing to be kind and forgiving. We must resist the knee-jerk reaction to respond in anger as the quick go-to emotion. We are called to seek peace over confusion.

Notice Jesus did not say blessed are the peacekeepers! A peacekeeper seeks to sustain peace by evading conflict and would usually attempt to steer clear of different positions to keep others content. A peacemaker is someone committed to resolving inner and outer chaos in order to establish peace with others and within themselves.

One can be a peacemaker even in protesting seeking to make every effort to keep the unity of the Spirit through the bond of peace. (Ephesians 4:3)

Jesus was a peacemaker but notice: He never avoided conflict. By His example, we can speak truth to power with appropriate passion and constraint. In fact, peacemaking is grace and mercy in action. A peacekeeper may have false illusions that everything is fine because of the absence of tension and conflict. However, that does not mean all is well. Neuropathy is a medical condition that can be masked by numbness; likewise one can be spiritually numb to the challenges among them.

A friend, Candys Mayo, shared Learn the difference between a leader and an instigator. Leaders deposit into the community that they serve, they spread a positive and encouraging message. They might even call you out on something you have done, but they do so privately and in a way that teaches and doesn't degrade. Thats agitation which is different from instigation. An instigator casts judgment, spreads rumors, negativity and withdraws energy from everyone else because they truly lack value, substance and creativity. They have to withdraw from others to cover up their own insecurities. Be a leader. Teach, don't tear down.

Michael Jacksons Man in the Mirror, with socially- conscious infused lyrics, If you want to make the world a better place, take a look at yourself and make a change!

You and I must foster environments of reconciliation where persons beyond race, gender, sexual orientation and faith can have civil, candid and courageous conversations about real differences as well as real agreements with the goal of establishing genuine relationships.

Who would disagree that our civil life is diminishing, especially in the political arena? When did it become standard for political discourse to turn into venomous and vitriol rancor? Who decided that insults are more potent than ideas? Hatred and discrimination should have no place in a civil society. Please realize this message is not meant to target any one individual as much as sharing a hope that we reject every act which demeans and derides others.

Can I make a personal pitch for civility? Let's agree to pledge to be more positive and polite while also having the willingness to confront offensive words with corrective action. Silence about incivility is not golden. Samuel Johnson, a philosopher once said When the forms of civility are violated, there remains little hope of a return to kindness or decency."

Understand, God is not going to hold others responsible for your decisions or responses to their actions. I often reflect upon the message was found written on the wall in Mother Teresa's home for children in Calcutta:

People are often unreasonable, irrational, and self-centered. Forgive them anyway.If you are kind, people may accuse you of selfish, ulterior motives. Be kind anyway.If you are successful, you will win some unfaithful friends and some genuine enemies. Succeed anyway.If you are honest and sincere people may deceive you. Be honest and sincere anyway.What you spend years creating, others could destroy overnight. Create anyway.If you find serenity and happiness, some may be jealous. Be happy anyway.The good you do today, will often be forgotten. Do good anyway.Give the best you have, and it will never be enough. Give your best anyway.In the final analysis, it is between you and God. It was never between you and them anyway.

Matthew 5: 43-44 reflects that People say love your neighbor and hate your enemy but I tell you to love your enemies and pray for anyone who mistreats you. Stop focusing on those you perceive are against you. In fact, loving your neighbor is easy-peasy! Its loving and praying for those who dislike you that is the real exercise. In many ways, treat your friend and your enemies with equal compassion, love and concern. After all, that's how God operates.

Notice its not about your feelings. Nor, should you feel good about having an enemy. However, it is always a decision of your will to respond proactively instead of reactively. Continuing this behavior as part of your lifestyle may ultimately result in that enemy becoming a friend.

Bishop Timothy J. Clarke First Church of God in Columbus references Psalms 23:5 to assert The Lord prepares a table before me in the presence of my enemies. Stop looking at your enemies and start focusing on your table. My table has love, mercy, provision, peace blessing! Why should I focus on my enemies where there is so much on my table?

So you dont have to force a smile or mutter softly as not to be heard to keep the peace. Own them but dont keep them! Those feelings when given the One full of grace is bright enough to melt in the light of His mercy as you endure and keep the faith.

Rev. Lewis W. Macklin II is the lead pastor of Holy Trinity Missionary Baptist Church, chaplain for the Youngstown Police Department and coordinator of the Mahoning Valley African American Male Wellness Walk. He resides in Youngstown with Dorothy, his partner in marriage and ministry. They share the love and joy of 5 children and 6 grandchildren.

All biblical references cited are New International Version unless otherwise noted.

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Global Diabetic Neuropathy Market 2020-2029 : Do You Really Need It? This Research Will Help You Decide! – News Monitoring

Sunday, July 12th, 2020

The Diabetic Neuropathy Market: Global Industry Analysis, Size, Share, Growth, Trends, and Forecasts 20202029 report covers all of the aspects required to gain a complete understanding of the pre-market conditions, current conditions as well as a well-measured forecast. This report also researches and evaluates the impact of the Covid-19 outbreak on the Diabetic Neuropathy Market, involving potential opportunity and challenges, drivers, and risks. We present the impact assessment of Covid-19 effects on Diabetic Neuropathy Market and market growth forecast based on different scenarios (optimistic, pessimistic, very optimistic, most likely, etc.).

The research report provides a comprehensive review of the global market. Analysts have identified the key drivers and restraints in the overall market. They have studied the historical milestones achieved by the global Diabetic Neuropathy Market and emerging trends. A comparison of the two has enabled the analysts to draw a potential trajectory of the global Diabetic Neuropathy Market for the forecast period.

For Better Understanding,Download FREE Exclusive PDF Sample Copy Of This Research Report:https://marketresearch.biz/report/diabetic-neuropathy-market/request-sample

For making the research report exhaustive, the analysts have included Porters five forces analysis and SWOT analysis. Both these assess the path the market is likely to take by factoring strengths, weaknesses, opportunities, and threats. Porters five forces analysis elucidates the intensity of the competitive rivalry and the bargaining power of suppliers and buyers. Furthermore, the research report also presents an in-depth explanation of the emerging trends in the global Diabetic Neuropathy Market and the disruptive technologies that could be key areas for investment.

Important Features that are under offering & key highlights of the report:

Detailed overview of Diabetic Neuropathy Market

Changing market dynamics of the Diabetic Neuropathy industry

In-depth Diabetic Neuropathy market segmentation by disorder type, treatment, and region etc

Historical, current and projected market size in terms of value and volume

Recent industry trends and developments

Competitive landscape of Diabetic Neuropathy Market

Strategies of key players and product/service offerings

Potential and niche segments/regions exhibiting promising growth

A neutral perspective towards Diabetic Neuropathy Market performance

Download FREE Sample PDF Report Here

Competition Analysis:

As the markets have been advancing the competition has increased by manifold and this has completely changed the way the competition is perceived and dealt with and in our report, we have discussed the complete analysis of the competition and how the big players in the Diabetic Neuropathy Market have been adapting to new techniques and what are the problems that they are facing.

Our research, which provides a comprehensive overview of mergers and acquisitions, will help you gain a full insight into market dynamics and will also give you a thorough knowledge of how to succeed and develop in the market.

The Leading Market Players Covered in this Report are:

Pfizer Inc, Eli Lilly and Company, Actavis Pharma Inc, Cephalon Inc, Meda Pharma GmbH, GlaxoSmithKline plc, NeuroMetrix Inc, Johnson & Johnson Inc, Boehringer Ingelheim GmbH, Astellas Pharma Inc

Global Diabetic Neuropathy Market Market: Segmentation

The chapters of segmentation allow the readers to understand the aspects of the market such as its products/service, available technologies, and applications of the same. The research report also offers valuable information on emerging developments that are likely to decide the success of these segments in the coming years.

Regions Covered in the Global Diabetic Neuropathy Market:

North America (the United States, Mexico, and Canada)

South America (Brazil etc.)

Europe (Germany, Turkey, Russia UK, France, Italy, etc.)

Asia-Pacific (Vietnam, China, Malaysia, Japan, Philippines, Korea, Thailand, India, Indonesia, and Australia)

The Middle East and Africa (GCC Countries and Egypt)

Inquire/Speak To Expert for Further Detailed Information About Diabetic Neuropathy Market Research Report:https://marketresearch.biz/report/diabetic-neuropathy-market/#inquiry

Table Of Content:

Chapter 1: Introduction, market driving force, product/service scope, market risk, overview, and opportunities of the global Diabetic Neuropathy Market

Chapter 2: Evaluating the leading players of the global Diabetic Neuropathy Market which consists of its revenue, sales, and price of the products

Chapter 3: Displaying the competitive nature among key players, with market share, revenue, and sales

Chapter 4: Presenting global Diabetic Neuropathy Market by regions, market share and with revenue and sales for the projected period

Chapter 5, 6, 7, 8 and 9: To evaluate the market by segments, by countries and by players with revenue share and sales by key countries in these various regions

GetDetailed Table Of Contents:https://marketresearch.biz/report/diabetic-neuropathy-market/#toc

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Diabetic Neuropathy Drugs Projected to be Resilient During 2019-2025 – Jewish Life News

Saturday, July 11th, 2020

Diabetic Neuropathy Drugs Market 2019: Global Industry Insights by Global Players, Regional Segmentation, Growth, Applications, Major Drivers, Value and Foreseen till 2024

The report provides both quantitative and qualitative information of global Diabetic Neuropathy Drugs market for period of 2019 to 2025. As per the analysis provided in the report, the global market of Diabetic Neuropathy Drugs is estimated to growth at a CAGR of _% during the forecast period 2019 to 2025 and is expected to rise to USD _ million/billion by the end of year 2025. In the year 2016, the global Diabetic Neuropathy Drugs market was valued at USD _ million/billion.

This research report based on Diabetic Neuropathy Drugs market and available with Market Study Report includes latest and upcoming industry trends in addition to the global spectrum of the Diabetic Neuropathy Drugs market that includes numerous regions. Likewise, the report also expands on intricate details pertaining to contributions by key players, demand and supply analysis as well as market share growth of the Diabetic Neuropathy Drugs industry.

Get PDF Sample Copy of this Report to understand the structure of the complete report: (Including Full TOC, List of Tables & Figures, Chart) @ https://www.marketresearchhub.com/enquiry.php?type=S&repid=2694284&source=atm

Diabetic Neuropathy Drugs Market Overview:

The Research projects that the Diabetic Neuropathy Drugs market size will grow from in 2019 to by 2024, at an estimated CAGR of XX%. The base year considered for the study is 2019, and the market size is projected from 2019 to 2024.

segment by Type, the product can be split intoCalcium Channel Alpha-2 Delta LigandSNRIs and TCAsOthersMarket segment by Application, split intoHospitalsDrug StoresOthers

Market segment by Regions/Countries, this report coversNorth AmericaEuropeChinaJapanSoutheast AsiaIndiaCentral & South America

The study objectives of this report are:To analyze global Diabetic Neuropathy Drugs status, future forecast, growth opportunity, key market and key players.To present the Diabetic Neuropathy Drugs development in North America, Europe, China, Japan, Southeast Asia, India and Central & South America.To strategically profile the key players and comprehensively analyze their development plan and strategies.To define, describe and forecast the market by type, market and key regions.

In this study, the years considered to estimate the market size of Diabetic Neuropathy Drugs are as follows:History Year: 2015-2019Base Year: 2019Estimated Year: 2020Forecast Year 2020 to 2026For the data information by region, company, type and application, 2019 is considered as the base year. Whenever data information was unavailable for the base year, the prior year has been considered.

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The Questions Answered by Diabetic Neuropathy Drugs Market Report:

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The report on the global Diabetic Neuropathy Drugs market covers 12 sections as given below:

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ECOFIBRE LIMITED Ananda Health products used in first FDA authorized clinical trial on hemp-derived CBD to treat chemotherapy induced peripheral…

Saturday, July 11th, 2020

Georgetown, Kentucky, July 07, 2020 (GLOBE NEWSWIRE) -- Ecofibre Limited (Ecofibre, Company) (ASX:EOF, OTC-NASDAQ Intl Designation: EOFBF) is pleased to announce that the Lankenau Institute for Medical Research1 (LIMR) has begun patient enrollment in a Phase II clinical trial using Ananda Health hemp-derived CBD.

The purpose of this study is to assess the efficacy of a hemp-based cannabidiol (CBD) product, Ananda Health Spectrum gelcaps, on the severity and duration of chemotherapy-induced peripheral neuropathy (CIPN) among breast, colon, and ovarian cancer patients who received common types of neurotoxic chemotherapy.

Ecofibre and Ananda demonstrate their commitment to advancing the science of CBD with the launch of the Coala-T-CBD study2 (ClinicalTrials.gov Identifier: NCT04398446). The phase II clinical trial began enrolling patients at LIMR in June.

The debilitating condition, CIPN, is often chronic, compromising patients quality of life and limiting their ability to complete a full course of potentially life-saving treatments. Currently, there are no safe and effective medications to treat or prevent CIPN, but research in animals using CBD offers hope as a new treatment.

The Coala-T-CBD StudyTMis the first clinical trial positioned to translate this success to humans and is led by oncologist Dr. Marisa Weiss, the founder and chief medical officer of http://www.Breastcancer.org and Director of Breast Radiation Oncology and Breast Health Outreach at Lankenau Medical Center.

We are proud to be the first in the United States to study the impact of hemp-derived full spectrum CBD on CIPN, a condition that affects approximately 25-50% of pediatric and adult cancer patients undergoing neurotoxic chemotherapy, Weiss states. Among other milestones, the Coala-T-CBD StudyTMreceived an IND (investigational new drug) by the Food and Drug Administration (FDA) and will use Ananda softgels in the study protocol.

To our knowledge, this is the first phase II clinical trial using full-spectrum hemp extract for the treatment of CIPN to receive an FDA IND. This level of research is necessary to answer the global call from the medical community, patients, and regulatory bodies seeking effective treatment of this difficult, common chemotherapy side effect, says Weiss. The IND allows for Weiss team to conduct the highest-quality research using a randomized, double-blind, placebo-controlled clinical trial.

Ananda Health Research Portfolio

The FDA has publicly requested data on hemp-derived CBD regarding tolerability, drug interactions, toxicity, and dosing. Ecofibre responded early by investing an additional USD $1.8 million in research across several studies.

In 2019, the company published a peer-reviewed study3regarding the effects of low-dose CBD in chronic pain patients. The results demonstrated that low-dose CBD was well tolerated and improved pain, sleep, mood and opioid use.

The Coala-T-CBD StudyTMcontributes to Ecofibres growing clinical research portfolio of CBD use across age groups, populations, disease states, and doses. Importantly, the Coala-T-CBD StudyTMwill offer critical insights on the use of higher-dose CBD.

Ecofibres second phase II clinical trial4(ClinicalTrials.gov Identifier: NCT04436081) will evaluate moderate-dose CBD on agitation, sleep and mood in dementia patients. The moderate-dose study is currently pursuing its own FDA IND and expects patient enrollment in August.

Both the Coala-T-CBD StudyTMand the dementia study include comprehensive physician and laboratory analyses to determine the safety of moderate and higher-dose CBD.

In addition to its clinical trials in the U.S., Ecofibre will be supporting research on low-dose full spectrum CBD later this year in Australia.

Alex Capano, Ecofibres Chief Science Officer states, These studies will provide solutions for patients and contribute valuable data on the safety and efficacy of hemp CBD products. We understand the critical need for more sophisticated, rigorous research and are dedicated to closing those gaps.

Ecofibre CEO, Eric Wang adds, A core foundation for Ananda Health has been to support quality research for patient and practitioner education. Whilst the recent pandemic has created market uncertainty, the Company remains highly committed to its long-term investment to support our customers and the FDA in creating the knowledge base to inform better decisions for our industry.

We are pleased to work with such a high-quality group of researchers and physicians at LIMR. The Coala-T-CBD StudyTMwill provide ongoing updates and anticipates completion in 2022.

For more information on Ecofibre Limited, visitwww.ecofibre.com.

About EcofibreEcofibre is a provider of hemp products in the United States and Australia.

In the United States, the Company produces nutraceutical products for human and pet consumption, as well as topical creams and salves. See http://www.anandahemp.com and http://www.anandaprofessional.com.

In Australia, the Company produces 100% Australian grown and processed hemp food products including protein powders, de-hulled hemp seed and hemp oil. See http://www.anandafood.com.

The Company is also developing innovative hemp-based products in textiles and composite materials in partnership with TexInnovate in the United States. See http://www.hempblack.com.

The Company owns or controls key parts of the value chain in each business, from breeding, growing and production to sales and marketing. Our value proposition to customers is built on strong brands and quality products.

About Main Line Health

Main Line Health is a not-for-profit health system serving portions of Philadelphia and its western suburbs. At its core are four of the regions most respected acute care hospitalsLankenau Medical Center, Bryn Mawr Hospital, Paoli Hospital and Riddle Hospitalas well as one of the nations premier facilities for rehabilitative medicine, Bryn Mawr Rehabilitation Hospital.

Main Line Health also includes the Lankenau Institute for Medical Research, a non-profit biomedical research organization on the campus of Lankenau Medical Center, dedicated to advancing an understanding of the causes of cancer, diabetes and heart disease to help improve diagnosis and treatment as well as prevention.

About Breastcancer.org

Breastcancer.org is a patient-centric resource for breast health and breast cancer information and support. Our research drives our ability to engage, educate, and empower people with breast cancer with expert information and dynamic peer support community to help them make the best decisions for their lives. The nonprofit organization was founded by breast oncologist Marisa C. Weiss, M.D. and born out of her conviction that women with breast cancer need more information and support than a physician visit can provide. Breastcancer.org receives more than 30 million visits each year. For more information about Breastcancer.org, please visit http://www.Breastcancer.org.

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2020 Insights into the Global Diabetic Neuropathy Industry – Market and Competitive Landscape – ResearchAndMarkets.com – Business Wire

Friday, July 10th, 2020

DUBLIN--(BUSINESS WIRE)--haThe "Global Diabetic Neuropathy Market and Competitive Landscape - 2020" report has been added to ResearchAndMarkets.com's offering.

This report provides comprehensive insights into the Diabetic Neuropathy pipeline, epidemiology, market valuations, drug sales, market forecast, drug forecasts, and market shares. This research analyzes and forecasts the Diabetic Neuropathy market size and drug sales. It also provides insights into Diabetic Neuropathy epidemiology and late stage pipeline.

This research covers the following: Diabetic Neuropathy treatment options, Diabetic Neuropathy late stage clinical trials pipeline, Diabetic Neuropathy prevalence by countries, Diabetic Neuropathy market size and forecast by countries, key market events and trends, drug sales and forecast by countries, and market shares by countries. The research scope includes the countries US, Germany, France, Italy, Spain, UK, Japan, Europe, Global (G7 Countries).

Research Scope:

Benefits of this Research:

Key Topics Covered:

1. Diabetic Neuropathy Treatment Options

2. Diabetic Neuropathy Pipeline Insights

2.1. Diabetic Neuropathy Phase 3 Clinical Trials

2.2. Diabetic Neuropathy Phase 2 Clinical Trials

2.3. Diabetic Neuropathy Phase 1 Clinical Trials

3. Diabetic Neuropathy Epidemiology Analysis by Countries

4. US Diabetic Neuropathy Market Insights

4.1. Marketed Drugs for Diabetic Neuropathy in US

4.2. US Diabetic Neuropathy Market Size & Forecast

4.3. US Diabetic Neuropathy Drugs Sales & Forecast

4.4. US Diabetic Neuropathy Market Share Analysis

5. Germany Diabetic Neuropathy Market Insights

5.1. Marketed Drugs for Diabetic Neuropathy in Germany

5.2. Germany Diabetic Neuropathy Market Size & Forecast

5.3. Germany Diabetic Neuropathy Drugs Sales Forecast

5.4. Germany Diabetic Neuropathy Market Share Analysis

6. France Diabetic Neuropathy Market Insights

6.1. Marketed Drugs for Diabetic Neuropathy in France

6.2. France Diabetic Neuropathy Market Size & Forecast

6.3. France Diabetic Neuropathy Product Sales Forecast

6.4. France Diabetic Neuropathy Market Share Analysis

7. Italy Diabetic Neuropathy Market Insights

7.1. Marketed Drugs for Diabetic Neuropathy in Italy

7.2. Italy Diabetic Neuropathy Market Size & Forecast

7.3. Italy Diabetic Neuropathy Product Sales Forecast

7.4. Italy Diabetic Neuropathy Market Share Analysis

8. Spain Diabetic Neuropathy Market Insights

8.1. Marketed Drugs for Diabetic Neuropathy in Spain

8.2. Spain Diabetic Neuropathy Market Size & Forecast

8.3. Spain Diabetic Neuropathy Product Sales Forecast

8.4. Spain Diabetic Neuropathy Market Share Analysis

9. UK Diabetic Neuropathy Market Insights

9.1. Marketed Drugs for Diabetic Neuropathy in UK

9.2. UK Diabetic Neuropathy Market Size & Forecast

9.3. UK Diabetic Neuropathy Product Sales Forecast

9.4. UK Diabetic Neuropathy Market Share Analysis

10. Europe Diabetic Neuropathy Market Insights

10.1. Europe Diabetic Neuropathy Market Size & Forecast

10.2. Europe Diabetic Neuropathy Product Sales Forecast

10.3. Europe Diabetic Neuropathy Market Share Analysis

11. Japan Diabetic Neuropathy Market Insights

11.1. Marketed Drugs for Diabetic Neuropathy in Japan

11.2. Japan Diabetic Neuropathy Market Size & Forecast

11.3. Japan Diabetic Neuropathy Product Sales Forecast

11.4. Japan Diabetic Neuropathy Market Share Analysis

12. Global Diabetic Neuropathy Market Insights

12.1. Global Diabetic Neuropathy Market Size & Forecast

12.2. Global Diabetic Neuropathy Product Sales Forecast

12.3. Global Diabetic Neuropathy Market Share Analysis

13. Research Methodology

For more information about this report visit https://www.researchandmarkets.com/r/vu5c4h

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2020 Insights into the Global Diabetic Neuropathy Industry - Market and Competitive Landscape - ResearchAndMarkets.com - Business Wire

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Real relief from neuropathy with Advanced Nerve and Health Center – KHOU.com

Thursday, July 9th, 2020

Janette Bowers lives with neuropathy and can now feel her feet again, thanks to Advanced Nerve and Health Center

HOUSTON Advanced Nerve and Health Center has a solution for those who suffer from nerve pain, or neuropathy. The treatment developed by Dr. Bao Thai is non-invasive, pain free and helps the body repair the nerves without surgery or medication.

The Advanced Nerve and Health Center has a limited time offer for Great Day Houston viewers. For $29, get a tele-health visit with a member of Dr. Thai's team, an in-office consultation, a copy of Dr. Thai's "Healthy Diet to Heal Nerve Pain" book, and a diagnostic nerve test to see if you are a good candidate for the process. This is a $249 value.

Call 832-626-1260 to book your appointment.

Advanced Nerve and Health Center is located at 8558 Katy Freeway, Suite 116, Houston, TX 77024.

For more information, log on to NerveAndHealth.com.

This content sponsored by Advanced Nerve and Health Center.

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Real relief from neuropathy with Advanced Nerve and Health Center - KHOU.com

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The Global Neuropathy Pain Treatment Market is expected to grow by $ 1702.89 mn during 2020-2024 progressing at a CAGR of 5% during the forecast…

Thursday, July 9th, 2020

Global Neuropathy Pain Treatment Market 2020-2024 The analyst has been monitoring the neuropathy pain treatment market and it is poised to grow by $ 1702. 89 mn during 2020-2024 progressing at a CAGR of 5% during the forecast period.

New York, July 07, 2020 (GLOBE NEWSWIRE) -- Reportlinker.com announces the release of the report "Global Neuropathy Pain Treatment Market 2020-2024" - https://www.reportlinker.com/p04796571/?utm_source=GNW Our reports on neuropathy pain treatment market provides a holistic analysis, market size and forecast, trends, growth drivers, and challenges, as well as vendor analysis covering around 25 vendors. The report offers an up-to-date analysis regarding the current global market scenario, latest trends and drivers, and the overall market environment. The market is driven by the presence of large patient pool and focus toward the development of novel therapeutics for postherpetic neuralgia. The neuropathy pain treatment market analysis includes type segment and geographic landscape.

The neuropathy pain treatment market is segmented as below: By Type Diabetic neuropathy Chemotherapy-induced neuropathy pain Postherpetic neuralgia Others

By Geographic Landscapes North America Europe APAC South America MEA

This study identifies the growing focus on the development of drugs for the treatment of diabetic neuropathy pain as one of the prime reasons driving the neuropathy pain treatment market growth during the next few years. The analyst presents a detailed picture of the market by the way of study, synthesis, and summation of data from multiple sources by an analysis of key parameters. Our neuropathy pain treatment market covers the following areas: Neuropathy pain treatment market sizing Neuropathy pain treatment market forecast Neuropathy pain treatment market industry analysis

Read the full report: https://www.reportlinker.com/p04796571/?utm_source=GNW

About ReportlinkerReportLinker is an award-winning market research solution. Reportlinker finds and organizes the latest industry data so you get all the market research you need - instantly, in one place.

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The Global Neuropathy Pain Treatment Market is expected to grow by $ 1702.89 mn during 2020-2024 progressing at a CAGR of 5% during the forecast...

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The Surging Demand for Ischemic Optic Neuropathy Treatment in Asia-Pacific Likely to Aid the Growth of the Ischemic Optic Neuropathy Treatment Market…

Thursday, July 9th, 2020

The Global Ischemic Optic Neuropathy Treatment market gives detailed Evaluation about all the Important aspects related to the marketplace. The analysis on global Ischemic Optic Neuropathy Treatment economy, offers profound insights regarding the Ischemic Optic Neuropathy Treatment market covering all of the crucial aspects of the market. Moreover, the report offers historical information with future prediction over the forecast period. Various important factors such as market trends, earnings growth patterns market shares and demand and supply are contained in almost all the market research report for every industry. A number of the vital facets analysed in the report contains market share, production, key regions, earnings rate in addition to key players.

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key players and product offerings

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A systematized methodology can be utilized to make a Report on the Global Ischemic Optic Neuropathy Treatment market. For the research of market on the terms of research Approaches, these techniques are useful. All of the Information Regarding the Products, manufacturers, vendors, clients and much more is covered in research reports. Various important factors like market trends, revenue Growth patterns market stocks and supply and demand are included in virtually all The market study report for every business. Adaptation of fresh ideas and Accepting the latest tendencies are a few the reasons for any markets growth. The Global Ischemic Optic Neuropathy Treatment market research report gives the deep understanding concerning the Regions where the market is impactful.

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The Surging Demand for Ischemic Optic Neuropathy Treatment in Asia-Pacific Likely to Aid the Growth of the Ischemic Optic Neuropathy Treatment Market...

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Diabetic Neuropathy Market Growth Opportunities by Regions, Scope, Key Players, Type and Application; Trend Forecast to 2026 – Daily Research…

Thursday, July 9th, 2020

The strategy analysis on Global Diabetic Neuropathy Market gives insights of market size, trends, share, growth, development plans, Investment Plan, cost structure and drivers analysis. With precise data covering all key aspects of the existing market, this report offers existing data of leading manufacturers. The Diabetic Neuropathy market report covers marketing channels and market positioning to potential growth strategies, providing in-depth analysis for new competitors or exists competitors in the Diabetic Neuropathy industry. The Report Gives Detail Analysis on Market concern Like Diabetic Neuropathy Market share, CAGR Status, Market demand and up to date Market Trends with key Market segments. The report provides key statistics on the market status of the Diabetic Neuropathy manufacturers and is a valuable source of guidance and direction for companies and individuals interested in the industry. Overall, the report provides an in-depth insight of Diabetic Neuropathy market covering all important parameters.

Note: *The Download PDF brochure only consist of Table of Content, Research Framework, and Research Methodology.

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Global Diabetic Neuropathy market 2020-2026: Competitive AnalysisThe Diabetic Neuropathy market report designed to provide entry support, customer profile and M&As as well as go-to-market strategy support. We provide a detailed analysis of key players operating in the global Diabetic Neuropathy market, including key players such as Eli Lilly and Company, GlaxoSmithKline, Pfizer, Johnson & Johnson and Janssen Pharmaceuticals.

Scope of Diabetic Neuropathy Market:

The Diabetic Neuropathy market was valued at XX Million US$ in 2019 and is projected to reach XX Million US$ by 2024, at a CAGR of XX% during the forecast period. In this study, 2019 has been considered as the base year and 2020 to 2024 as the forecast period to estimate the market size for Diabetic Neuropathy.

Due to the pandemic, we have included a special section on the Impact of COVID 19 on the Diabetic Neuropathy Market which would mention How the Covid-19 is Affecting the Diabetic Neuropathy Industry, Market Trends and Potential Opportunities in the COVID-19 Landscape, Covid-19 Impact on Key Regions and Proposal for Diabetic Neuropathy Players to fight Covid-19 Impact.

The report also focuses on global major leading industry players of Global Diabetic Neuropathy market providing information such as company profiles, product picture and specification, price, capacity, cost, production, revenue and contact information. Upstream raw materials and equipment and downstream demand analysis are also carried out. With tables and figures helping analyze worldwide Global Diabetic Neuropathy market, this research provides key statistics on the state of the industry and is a valuable source of guidance and direction for companies and individuals interested in the market. In general, the research report is a compilation of key data with regards to the competitive landscape of this vertical and the multiple regions where the business has successfully established its position. The report provides detailed information regarding the major factors (drivers, restraints, opportunities, and challenges) influencing the growth of the Diabetic Neuropathy market. The Diabetic Neuropathy Market Report analyzes opportunities in the overall Diabetic Neuropathy market for stakeholders by identifying the high growth segments.

The scope of the report is limited to the application of the type, and distribution channel. The regions considered in the scope of the report include North America Country (United States, Canada), South America, Asia Country (China, Japan, India, Korea), Europe Country (Germany, UK, France, Italy), Other Country (Middle East, Africa, GCC). This report presents the worldwide Diabetic Neuropathy market size (value, production and consumption), splits the breakdown (data status 20152019 and forecast to 2024), by manufacturers, region, type and application.

Market segment by Type, the product can be split into:Product Type Segmentation: Epicel, IntegraIndustry Segmentation: Chemical, Cosmetic, Pharmaceutical

The Global Diabetic Neuropathy Market report analyses the production of goods, supply, sales, and the current status of the market in a detailed manner. Furthermore, the report examines the production shares and market product sales, as well as the capacity, production capacity, trends in sales, cost analysis, and revenue generation. Several other factors such as import/export status, industrial statistics, demand and supply ratio, gross margin, and industry chain structure have also been studied in the Global Diabetic Neuropathy Market report.

The report comprehends precise analytical information related to market forecasts for several upcoming years. The report also includes the particulars about the valuation of macro and microelements significant for the growth of already established Diabetic Neuropathy Market contenders and emerging new companies. The report uses SWOT analysis for the growth assessment of the outstanding Diabetic Neuropathy Market players. It also analyzes the most recent enhancements while estimating the expansion of the foremost Diabetic Neuropathy Market players. Additionally, the key product category and segments along with sub-segments of the global Diabetic Neuropathy Market are studied in the global Market research.

What Reports Provides

Full in-depth analysis of the parent market Important changes in market dynamics Segmentation details of the market Former, on-going, and projected market analysis in terms of volume and value Assessment of niche industry developments Market share analysis Key strategies of major players Emerging segments and regional markets Testimonials to companies in order to fortify their foothold in the market.

Further, in the research report, the following points are included along with an in-depth study of each point:

* Production Analysis Production is analyzed with respect to different regions, types, and applications. Here, the price analysis of various Market key players is also covered.* Sales and Revenue Analysis Both, sales and revenue are studied for the different regions of the global market. Another major aspect, price, which plays an important part in the revenue generation is also assessed in this section for the various regions.* Supply and Consumption In continuation of sales, this section studies the supply and consumption of the Market. This part also sheds light on the gap between supply and consumption. Import and export figures are also given in this part.* Other analyses Apart from the information, trade and distribution analysis for the Market, contact information of major manufacturers, suppliers and key consumers are also given. Also, SWOT analysis for new projects and feasibility analysis for new investment are included.

Reasons to Buy:

* Obtain the most up to date information available on the Diabetic Neuropathy projects globally.* Identify growth segments and opportunities in the industry.* Facilitate decision-making on the basis of strong historical and outlook of Diabetic Neuropathy data.* Develop business strategies with the help of specific insights about the planned and announced Diabetic Neuropathy projects globally.* Keep abreast of key new-build Diabetic Neuropathy projects globally.* Assess your competitors planned and Diabetic Neuropathy projects and capacities.

Additionally, the report is joined by a vital examination of the Diabetic Neuropathy marketplace considering progress, part commitments, and future market forecasts. Furthermore, it offers detailed data of vendors including the profile, specifications of a product, sales, applications, annual performance in the industry, investments, acquisitions and mergers, market size, revenue, market share, and more. The report also studies individual regional market size along with country-wise and region-wise market size during the forecast period. The report also understands the export and import, production, and consumption of every particular region holding the highest market share, market size, or CAGR.

Conclusively, This report will provide you a clear view of each and every fact of the market without a need to refer to any other research report or a data source. Our report will provide you with all the facts about the past, present, and future of the concerned Market.

Note: *The discount is offered on the Standard Price of the report.

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Diabetic Neuropathy Market Growth Opportunities by Regions, Scope, Key Players, Type and Application; Trend Forecast to 2026 - Daily Research...

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Diabetic Neuropathy Therapeutics Market: Forecast With Size, Share, Analysis, Rising Demand and Opportunity Outlook: Abbott Laboratories, Hoffmann-La…

Thursday, July 9th, 2020

Diabetic Neuropathy Therapeutics Market has witnessed continuous growth within the past few years and is projected to grow even more throughout the forecast period (2020 2027). The analysis presents a whole assessment of the market and contains Future trends, Current Growth Factors, attentive opinions, facts, historical information, and statistically supported and trade valid market information.

The report, titled Global Diabetic Neuropathy Therapeutics Market defines and briefs readers about its products, applications, and specifications. The research lists key companies operating in the global market and also highlights the key changing trends adopted by the companies to maintain their dominance. By using SWOT analysis and Porters five force analysis tools, the strengths, weaknesses, opportunities, and threats of key companies are all mentioned in the report. All leading players in this global market are profiled with details such as product types, business overview, sales, manufacturing base, competitors, applications, and specifications.

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Abbott Laboratories, Hoffmann-La Roche Ltd, Eli Lilly and Company, Johnson & Johnson, GlaxoSmithKline Plc, Lupin Limited, Glenmark Pharmaceuticals Limited, Depomed Inc., Astellas Pharma Inc, Pfizer Inc of the major organizations dominating the global market.(*Note: Other Players Can be Added per Request)

1. Industry outlookThis is where youll find the current state of the Diabetic Neuropathy Therapeutics industry overall and where its headed. Relevant industry metrics like size, trends, life cycle, and projected growth included here. This report comes prepared with the data to back up your business idea. On a regional basis, the Global Diabetic Neuropathy Therapeutics market has been segmented into Asia-Pacific, North America, Europe, Latin America, and the Middle East and Africa.

2. Target marketThis target market section of study includes the following:

User persona and characteristics: It includes demographics such as age, income, and location. It lets you know what their interests and buying habits are, as well as explain the best position to meet their needs.

Market size: How big is the potential Diabetic Neuropathy Therapeutics market for your business? It brings to light the consumption in the Diabetic Neuropathy Therapeutics industry by the type and application.

3. Competitive analysisDiscover your competitors. The report lets you know what youre up against, but it also lets you spot the competitions weaknesses. Are there customers that are underserved? What can you offer that similar businesses arent offering? The competitive analysis contains the following components:

Direct competitors: What other companies are offering similar products and services? Which companies are your true competitors?

Competitor strengths and weaknesses: What is your competition good at? Where do they fall behind? Get insights to spot opportunities to excel where others are falling short.

Barriers to entry: What are the potential pitfalls of entering the Diabetic Neuropathy Therapeutics market? Whats the cost of entry? Is it prohibitively high, or easy to enter?

The window of opportunity:Does your entry into the Diabetic Neuropathy Therapeutics industry rely on time-sensitive technology? Do you need to enter early to take advantage of an emerging market?

4. ProjectionsLikewise, We offered thoughtful, not hockey-stick forecasting.

Market share:We have given the consumption behavior of users. When you know how much can your future customers spend, then only youll understand how much of the Diabetic Neuropathy Therapeutics industry you have a chance to grab, and here we came up with real stats and numbers.

Impact Analysis of COVID-19:The complete version of the Report will include the impact of the COVID-19, and anticipated change on the future outlook of the industry, by taking into account the political, economic, social, and technological parameters.

Finally, It is one report that hasnt shied away from taking a critical look at the current status and future outlook for the consumption/sales of these products, by the end users and applications. Not forgetting the market share control and growth rate of the Diabetic Neuropathy Therapeutics Industry, per application. Most noteworthy, this market analysis will help you find market blind spots.

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Worldwide Market Reports is your one-stop repository of detailed and in-depth market research reports compiled by an extensive list of publishers from across the globe. We offer reports across virtually all domains and an exhaustive list of sub-domains under the sun. The in-depth market analysis by some of the most vastly experienced analysts provide our diverse range of clients from across all industries with vital decision making insights to plan and align their market strategies in line with current market trends.

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Chemotherapy Induced Peripheral Neuropathy Treatment Market Is Set To Experience Revolutionary Growth By 2025 – Jewish Life News

Monday, July 6th, 2020

A report on Chemotherapy Induced Peripheral Neuropathy Treatment market compiled by Brand Essence Market Research provides a succinct analysis regarding the values and trends existing in the current business scenario. The study also offers a brief summary of market valuation, market size, regional outlook and profit estimations of the industry. Furthermore, the report examines the competitive sphere and growth strategies of leading players in the Chemotherapy Induced Peripheral Neuropathy Treatment market.

In 2018, the GlobalChemotherapy Induced Peripheral Neuropathy Treatment Marketsize was xx million US$ and it is expected to reach xx million US$ by the end of 2025, with a CAGR of xx% during 2019-2025.

Download Premium Sample of the Report:https://industrystatsreport.com/Request/Sample?ResearchPostId=389&RequestType=Sample

Key playersof the Chemotherapy Induced Peripheral Neuropathy Treatment market are Aptinyx, AsahiKaseiPharma, RegenacyPharmaceuticals, MAKScientific, MetysPharmaceuticals, NemusBioscience, PledPharma, SovaPharmaceuticals, DermaXon, ImmunePharmaceuticals, Kineta, KrenitskyPharmaceuticals, PeriphaGen, ApexianPharma, WinSanTor, SolasiaPharma

Chemotherapy Induced Peripheral Neuropathy Treatment Market Segmentation:

Reports include the following segmentation: By ProductCalcium Channel ?2-delta LigandsAntidepressantsOpioidsOthersBy ApplicationsPlatinum AgentsTaxanesVinca AlkaloidsOthersBy RegionNorth Americao U.S.o Canadao MexicoEuropeo UKo Franceo Germanyo Russiao Rest of EuropeAsia-Pacifico Chinao South Koreao Indiao Japano Rest of Asia-PacificLAMEAo Latin Americao Middle Easto Africa

Region Coverage (Regional Production, Demand & Forecast by Countries etc.):North America (U.S., Canada, Mexico)Europe (Germany, U.K., France, Italy, Russia, Spain etc.)Asia-Pacific (China, India, Japan, Southeast Asia etc.)South America (Brazil, Argentina etc.)Middle East & Africa (Saudi Arabia, South Africa etc.)

Table of Contents

1 Report Overview1.1 Study Scope1.2 Key Market Segments1.3 Players Covered1.4 Market Analysis by Type1.4.1 Global Chemotherapy Induced Peripheral Neuropathy Treatment Market Size Growth Rate by Type (2014-2025)1.4.2 Topical Products1.4.3 Botulinum1.4.4 Dermal Fillers1.4.5 Chemical Peels1.4.6 Microabrasion Equipment1.4.7 Laser Surfacing Treatments1.5 Market by Application1.5.1 Global Chemotherapy Induced Peripheral Neuropathy Treatment Market Share by Application (2014-2025)1.5.2 Hospitals1.5.3 Dermatology Clinics1.6 Study Objectives1.7 Years Considered

2 Global Growth Trends2.1 Chemotherapy Induced Peripheral Neuropathy Treatment Market Size2.2 Chemotherapy Induced Peripheral Neuropathy Treatment Growth Trends by Regions2.2.1 Chemotherapy Induced Peripheral Neuropathy Treatment Market Size by Regions (2014-2025)2.2.2 Chemotherapy Induced Peripheral Neuropathy Treatment Market Share by Regions (2014-2019)2.3 Industry Trends2.3.1 Market Top Trends2.3.2 Market Drivers2.3.3 Market Opportunities

3 Market Share by Key Players3.1 Chemotherapy Induced Peripheral Neuropathy Treatment Market Size by Manufacturers3.1.1 Global Chemotherapy Induced Peripheral Neuropathy Treatment Revenue by Manufacturers (2014-2019)3.1.2 Global Chemotherapy Induced Peripheral Neuropathy Treatment Revenue Market Share by Manufacturers (2014-2019)3.1.3 Global Chemotherapy Induced Peripheral Neuropathy Treatment Market Concentration Ratio (CR5 and HHI)3.2 Chemotherapy Induced Peripheral Neuropathy Treatment Key Players Head office and Area Served3.3 Key Players Chemotherapy Induced Peripheral Neuropathy Treatment Product/Solution/Service3.4 Date of Enter into Chemotherapy Induced Peripheral Neuropathy Treatment Market3.5 Mergers & Acquisitions, Expansion Plans

Read More:https://industrystatsreport.com/Medical-Devices-and-Consumables/Chemotherapy-Induced-Peripheral-Neuropathy-Treatment-Market-Size/Summary

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Brandessence market research publishes market research reports & business insights produced by highly qualified and experienced industry analysts. Our research reports are available in a wide range of industry verticals including aviation, food & beverage, healthcare, ICT, Construction, Chemicals and lot more. Brand Essence Market Research report will be best fit for senior executives, business development managers, marketing managers, consultants, CEOs, CIOs, COOs, and Directors, governments, agencies, organizations and Ph.D. Students. We have a delivery center in Pune, India and our sales office is in London.

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Analysis of COVID-19 Impact: Neuropathy Pain Treatment Market 2020-2024 | Presence of Large Patient Pool to Augment Growth | Technavio – Business Wire

Monday, July 6th, 2020

LONDON--(BUSINESS WIRE)--Technavio has been monitoring the neuropathy pain treatment market and it is poised to grow by USD 1,702.89 million during 2020-2024, progressing at a CAGR of almost 5% during the forecast period. The report offers an up-to-date analysis regarding the current market scenario, latest trends and drivers, and the overall market environment.

Although the COVID-19 pandemic continues to transform the growth of various industries, the immediate impact of the outbreak is varied. While a few industries will register a drop in demand, numerous others will continue to remain unscathed and show promising growth opportunities. Technavios in-depth research has all your needs covered as our research reports include all foreseeable market scenarios, including pre- & post-COVID-19 analysis. Download a Free Sample Report

The market is fragmented, and the degree of fragmentation will accelerate during the forecast period. Abbott Laboratories, Assertio Therapeutics Inc., AstraZeneca Plc, Baxter International Inc., Eli Lilly and Co., Endo International Plc, Johnson & Johnson, Pfizer Inc., and Sanofi are some of the major market participants. To make the most of the opportunities, market vendors should focus more on the growth prospects in the fast-growing segments, while maintaining their positions in the slow-growing segments.

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View market snapshot before purchasing

The presence of a large patient pool has been instrumental in driving the growth of the market. However, growing preference for alternatives and high unmet needs in the treatment of neuropathic pain might hamper the market growth.

Technavio's custom research reports offer detailed insights on the impact of COVID-19 at an industry level, a regional level, and subsequent supply chain operations. This customized report will also help clients keep up with new product launches in direct & indirect COVID-19 related markets, upcoming vaccines and pipeline analysis, and significant developments in vendor operations and government regulations.

Neuropathy Pain Treatment Market 2020-2024: Segmentation

Neuropathy Pain Treatment Market is segmented as below:

To learn more about the global trends impacting the future of market research, download a free sample: https://www.technavio.com/talk-to-us?report=IRTNTR43322

Neuropathy Pain Treatment Market 2020-2024: Scope

Technavio presents a detailed picture of the market by the way of study, synthesis, and summation of data from multiple sources. The neuropathy pain treatment market report covers the following areas:

This study identifies the growing focus on the development of drugs for the treatment of diabetic neuropathy pain as one of the prime reasons driving the neuropathy pain treatment market growth during the next few years.

Technavio suggests three forecast scenarios (optimistic, probable, and pessimistic) considering the impact of COVID-19. Technavios in-depth research has direct and indirect COVID-19 impacted market research reports.

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Neuropathy Pain Treatment Market 2020-2024: Key Highlights

Table of Contents:

Executive Summary

Market Landscape

Market Sizing

Five Forces Analysis

Market Segmentation by Indication

Market Segmentation by Drug Class

Customer landscape

Geographic Landscape

Vendor Landscape

Vendor Analysis

Appendix

About Us

Technavio is a leading global technology research and advisory company. Their research and analysis focus on emerging market trends and provides actionable insights to help businesses identify market opportunities and develop effective strategies to optimize their market positions. With over 500 specialized analysts, Technavios report library consists of more than 17,000 reports and counting, covering 800 technologies, spanning across 50 countries. Their client base consists of enterprises of all sizes, including more than 100 Fortune 500 companies. This growing client base relies on Technavios comprehensive coverage, extensive research, and actionable market insights to identify opportunities in existing and potential markets and assess their competitive positions within changing market scenarios.

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Analysis of COVID-19 Impact: Neuropathy Pain Treatment Market 2020-2024 | Presence of Large Patient Pool to Augment Growth | Technavio - Business Wire

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New Comprehensive Report on Neuropathy Pain Treatment Market to Witness an Outstanding Growth during 2020 2025 with Top Players Like Pfizer, Depomed,…

Monday, July 6th, 2020

Overview Of Neuropathy Pain Treatment Industry 2020-2025:

This has brought along several changes in This report also covers the impact of COVID-19 on the global market.

The Neuropathy Pain Treatment Market analysis summary by Reports Insights is a thorough study of the current trends leading to this vertical trend in various regions. Research summarizes important details related to market share, market size, applications, statistics and sales. In addition, this study emphasizes thorough competition analysis on market prospects, especially growth strategies that market experts claim.

Neuropathy Pain Treatment Market competition by top manufacturers as follow: , Pfizer, Depomed, Eli Lilly, Endo, Grnenthal Group, Arbor Pharmaceuticals

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The global Neuropathy Pain Treatment market has been segmented on the basis of technology, product type, application, distribution channel, end-user, and industry vertical, along with the geography, delivering valuable insights.

The Type Coverage in the Market are: Calcium channel alpha 2-delta ligandsSerotonin-norepinephrine reuptake inhibitorsOthers

Market Segment by Applications, covers:Retail PharmaciesHospitals

Market segment by Regions/Countries, this report coversNorth AmericaEuropeChinaRest of Asia PacificCentral & South AmericaMiddle East & Africa

Major factors covered in the report:

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The analysis objectives of the report are:

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New Comprehensive Report on Neuropathy Pain Treatment Market to Witness an Outstanding Growth during 2020 2025 with Top Players Like Pfizer, Depomed,...

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Diabetic Neuropathy Drugs Market Growth By Manufacturers, Type And Application, Forecast To 2026 – 3rd Watch News

Monday, July 6th, 2020

New Jersey, United States,- Market Research Intellect sheds light on the market scope, potential, and performance perspective of the Global Diabetic Neuropathy Drugs Market by carrying out an extensive market analysis. Pivotal market aspects like market trends, the shift in customer preferences, fluctuating consumption, cost volatility, the product range available in the market, growth rate, drivers and constraints, financial standing, and challenges existing in the market are comprehensively evaluated to deduce their impact on the growth of the market in the coming years. The report also gives an industry-wide competitive analysis, highlighting the different market segments, individual market share of leading players, and the contemporary market scenario and the most vital elements to study while assessing the global Diabetic Neuropathy Drugs market.

The research study includes the latest updates about the COVID-19 impact on the Diabetic Neuropathy Drugs sector. The outbreak has broadly influenced the global economic landscape. The report contains a complete breakdown of the current situation in the ever-evolving business sector and estimates the aftereffects of the outbreak on the overall economy.

Leading Diabetic Neuropathy Drugs manufacturers/companies operating at both regional and global levels:

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The Diabetic Neuropathy Drugs market report provides successfully marked contemplated policy changes, favorable circumstances, industry news, developments, and trends. This information can help readers fortify their market position. It packs various parts of information gathered from secondary sources, including press releases, web, magazines, and journals as numbers, tables, pie-charts, and graphs. The information is verified and validated through primary interviews and questionnaires. The data on growth and trends focuses on new technologies, market capacities, raw materials, CAPEX cycle, and the dynamic structure of the Diabetic Neuropathy Drugs market.

This study analyzes the growth of Diabetic Neuropathy Drugs based on the present, past and futuristic data and will render complete information about the Diabetic Neuropathy Drugs industry to the market-leading industry players that will guide the direction of the Diabetic Neuropathy Drugs market through the forecast period. All of these players are analyzed in detail so as to get details concerning their recent announcements and partnerships, product/services, and investment strategies, among others.

Sales Forecast:

The report contains historical revenue and volume that backing information about the market capacity, and it helps to evaluate conjecture numbers for key areas in the Diabetic Neuropathy Drugs market. Additionally, it includes a share of each segment of the Diabetic Neuropathy Drugs market, giving methodical information about types and applications of the market.

Reasons for Buying Diabetic Neuropathy Drugs Market Report

This report gives a forward-looking prospect of various factors driving or restraining market growth.

It renders an in-depth analysis for changing competitive dynamics.

It presents a detailed analysis of changing competition dynamics and puts you ahead of competitors.

It gives a six-year forecast evaluated on the basis of how the market is predicted to grow.

It assists in making informed business decisions by performing a pin-point analysis of market segments and by having complete insights of the Diabetic Neuropathy Drugs market.

This report helps the readers understand key product segments and their future.

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In the end, the Diabetic Neuropathy Drugs market is analyzed for revenue, sales, price, and gross margin. These points are examined for companies, types, applications, and regions.

To summarize, the global Diabetic Neuropathy Drugs market report studies the contemporary market to forecast the growth prospects, challenges, opportunities, risks, threats, and the trends observed in the market that can either propel or curtail the growth rate of the industry. The market factors impacting the global sector also include provincial trade policies, international trade disputes, entry barriers, and other regulatory restrictions.

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Diabetic Neuropathy Drugs Market Growth By Manufacturers, Type And Application, Forecast To 2026 - 3rd Watch News

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Chemotherapy Induced Peripheral Neuropathy Treatment Market 2026 Expected to reach Highest CAGR including major key players Achelios Therapeutics Inc,…

Monday, July 6th, 2020

Due to the pandemic, we have included a special section on the Impact of COVID 19 on the Chemotherapy Induced Peripheral Neuropathy TreatmentMarket which would mention How the Covid-19 is Affecting the Industry, Market Trends and Potential Opportunities in the COVID-19 Landscape, Key Regions and Proposal for Chemotherapy Induced Peripheral Neuropathy Treatment Market Players to battle Covid-19 Impact.

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Calpain-2 as a therapeutic target in repeated concussioninduced neuropathy and behavioral impairment – Science Advances

Monday, July 6th, 2020

Abstract

Repeated concussion represents a serious health problem as it can result in various brain pathologies, ranging from minor focal tissue injury to severe chronic traumatic encephalopathy. The calcium-dependent protease, calpain, participates in the development of neurodegeneration following concussion, but there is no information regarding the relative contribution of calpain-1 and calpain-2, the major calpain isoforms in the brain. We used a mouse model of repeated concussions, which reproduces most of the behavioral and neuropathological features of the human condition, to address this issue. Deletion of calpain-2 or treatment with a selective calpain-2 inhibitor for 2 weeks prevented most of these neuropathological features. Changes in TAR DNA binding protein 43 (TDP-43) subcellular localization similar to those found in human amyotrophic lateral sclerosis and frontotemporal dementia were also prevented by deletion of calpain-2 or treatment with calpain-2 inhibitor. Our results indicate that a selective calpain-2 inhibitor represents a therapeutic approach for concussion.

Traumatic brain injury (TBI) is a serious public health problem in the United States. In 2013 alone, an estimated 2.8 million TBI cases presented for treatment, and it is likely that many more cases were never reported (www.cdc.gov/traumaticbraininjury/get_the_facts.html). The cause of injury varies greatly and includes motor vehicle accidents, falls, sport injuries, and gunshot wounds, to name a few. The severity of TBI is generally classified as mild (1), also called concussion, moderate, and severe, which is often associated with a prolonged period of unconsciousness after the injury. TBI induces immediate and prolonged neuropathological consequences, including axonal damage (2) and neuronal death (3). In recent years, repeated mild TBI (rmTBI) has received a lot of attention after it was found that many athletes subjected to repeated concussions exhibit a chronic degenerative disease referred to as chronic traumatic encephalopathy (CTE) (4). CTE is characterized by massive accumulation of hyperphosphorylated tau, gliosis, and neurodegeneration (5).

Numerous reviews have discussed the role of calpain in neurodegeneration (6, 7) in general and more specifically, in stroke (8, 9) and TBI (10, 11). Consequently, numerous studies have evaluated the use of calpain inhibitors to reduce neurodegeneration in both stroke and TBI (12, 13, 14). While some studies have reported some positive effects of calpain inhibitors in TBI (15), other studies have not confirmed these results. In particular, overexpression of the endogenous calpain inhibitor, calpastatin, was reported to reduce the formation of spectrin breakdown product (SBDP) (9), resulting from calpain-mediated truncation of spectrin, a widely used biomarker of calpain activation and potentially of neurodegeneration (16), but had no effect on neurodegeneration (17). Recent studies concluded that two calpain inhibitors, SNJ-1945 and MDL-28170, which are blood-brain barrier and cell permeable, did not have sufficient efficacy or a practical therapeutic window in a widely used TBI model, referred to as the controlled cortical impact (CCI) model (15, 18). While those nonisoform-selective calpain inhibitors were shown to inhibit overall calpain activation (without distinguishing which calpain isoform was targeted) following TBI, they failed to provide neuroprotection.

Diffuse axonal degeneration has been shown to be responsible for many of the long-term functional consequences of mTBI (1, 19). Calpain activation has been repeatedly shown to be involved in diffuse axonal injury, as calpain-mediated proteolysis of spectrin has been observed 1 to 2 hours after injury. Blood levels of the calpain-mediated N-terminal fragment of spectrin were found to be elevated shortly after injury and predicted the long-term consequences of the injury in patients with mTBI, including professional hockey players experiencing concussions (20, 21). While all the evidence strongly supports a role for calpain in mTBI, there is little information regarding which of the calpain isoforms is responsible for producing the neuropathological consequences of mTBI or rmTBI. We previously proposed that calpain-1 activation was neuroprotective, while calpain-2 activation was neurodegenerative and provided evidence for such opposite functions of these two calpain isoforms in the CCI mouse model of TBI (22). Here, we report that calpain-2 conditional knockout (C2CKO) mice are remarkably protected against the pathological consequences of rmTBI. Moreover, semichronic treatment of wild-type (WT) mice with a selective calpain-2 inhibitor results in a similar level of protection in the rmTBI mouse model. In this model, the amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD) marker, TDP-43, exhibits changes in subcellular localization similar to those found in these patients, and these changes are also prevented by either genetic deletion or pharmaceutical inhibition of calpain-2. These results strongly suggest that a selective calpain-2 inhibitor could be a useful therapeutic treatment to prevent the long-term consequences of repeated concussions.

We generated C2CKO mice by crossing loxPcalpain-2 mice (obtained from the Riken Institute, Japan) with CamKII-Cre mice (the Jackson laboratory) to produce mice with selective calpain-2 deletion in excitatory neurons from the forebrain. These mice exhibit widespread deletion of calpain-2 in the majority of neurons in the cortex and almost complete elimination of calpain-2 in hippocampus (Fig. 1A and fig. S1A). We previously reported that N-methyl-d-aspartate (NMDA)mediated neurotoxicity in acute hippocampal slices prepared from juvenile mice was exacerbated in calpain-1 KO mice but reduced in the presence of a calpain-2 inhibitor (23). To further corroborate the role of calpain-2 in NMDA-mediated neurotoxicity, we tested the effects of NMDA treatment of hippocampal slices from 2-week-old WT or from C2CKO mice on neuronal injury. As previously reported, NMDA treatment resulted in a significant increase in lactate dehydrogenase (LDH) release in the incubation medium, a well-recognized marker of neurotoxicity (Fig. 1B). The effect was significantly reduced in the slices from C2CKO mice, thereby confirming the role of calpain-2 activation in NMDA-mediated neurotoxicity. NMDA receptormediated neurotoxicity has been extensively studied in TBI models (24). We compared the extent of brain lesion in WT and C2CKO mice in the CCI model of TBI. Lesion volume was significantly reduced in the brain of C2CKO mice as compared to WT mice (fig. S1, B and C). These results further support the role of calpain-2 activation in NMDA receptormediated neurotoxicity in vivo.

(A) Calpain-2 deletion in cortex and hippocampus in C2CKO mice. loxP-Calpain-2 mice were crossed with CamKII-Cre mice to generate mice with calpain-2 deletion in excitatory neurons of the forebrain. Note the very large decrease in calpain-2 immunoreactivity in cortex and field CA1 of hippocampus and the absence of changes in calpain-1 staining. Scale bar, 50 m. (B) Reduced NMDA-mediated toxicity in acute hippocampal slices from C2CKO mice. Hippocampal slices were prepared from 3-week-old WT or C2CKO mice. They were incubated with NMDA (100 M) for 2.5 hours, and lactate dehydrogenase (LDH) release in the medium was assayed. Results represent means SEM of four experiments. **P < 0.01. Two-way analysis of variance (ANOVA) followed by Bonferronis test. (C and F) Changes in spectrin and TDP-43 in ipsilateral cortex (C) and hippocampus (F) at various times after the last concussion in WT and C2CKO mice. WT and C2CKO mice were subjected to 10 days of repeated concussions. They were sacrificed 1, 3, and 7 days after the last day of treatment, and levels of the SBDP generated by calpain activation and full-length TDP-43 were determined by Western blot analysis. (D, E, and G) Quantification of the Western blot data for ipsilateral cortex [(D) and (E)] and ipsilateral hippocampus (G). Results represent means SEM of four experiments. *P < 0.05, **P < 0.01 compared to WT basal. Two-way ANOVA followed by Bonferronis test. Ctl, control.

We previously reported that calpain-2 played a significant role in the CCI model of TBI in mice (22). To analyze the potential role of calpain-2 in rmTBI, we used the repetitive concussion model developed by Petraglia and colleagues (25, 26). In this model, awake mice are subjected to four daily hits on the head for 10 consecutive days (see Materials and Methods). We first determined the time course of calpain activation in the brain in this model. Animals were sacrificed at various times after the last impact, and levels of the SBDP generated by calpain activation in cortex and hippocampus were determined (Fig. 1, C to F). In WT mice, SBDP levels in the cortex ipsilateral from the impact were elevated 24 hours and 3 days after the last impact. They were still slightly elevated 7 days after the last impact. Similar results were found in ipsilateral hippocampus. In contrast, there was no increase in SBDP levels at any time in cortex or hippocampus from C2CKO mice. We also analyzed the time course of the exposure of the phosphatase-activated domain (PAD) of tau, which appears early in tauopathy (fig. S1, D to G) (27, 28). In control animals, the changes in PAD-tau were quite similar to those found in SBDP in both cortex and hippocampus, with small variation in statistical significance. In contrast, there were no changes in phosphoPAD-tau in cortex and hippocampus from C2CKO mice after rmTBI.

Previous studies using the same model of repeated concussions have shown that mice exhibited a number of behavioral impairments, including cognitive impairment, as well as many pathological changes, such as activation of astrocytes and microglia in various brain regions and axonal degeneration mostly localized to the corpus callosum and the optic tract (24). At 1 and 3 months after the last concussion, WT mice exhibited depressed behavior after the last concussion, as evidenced in the tail suspension test in which mice subjected to repeated concussions became immobile much faster than the sham mice (Fig. 2, A and B); in contrast, C2CKO mice did not exhibit any of these behavioral alterations. We also tested the loxP-calpain-2 mice (control for C2CKO) and found that they behave very similarly to the WT mice. At 1 and 3 months after repeated concussions, WT mice exhibited increased risk-taking behavior in the elevated plus maze, as evidenced by increased time spent in the open arms and increased number of entries in open arms (Fig. 2, C to F). This behavioral alteration was completely absent in C2CKO mice. Again, control mice behave similarly to WT mice. Last, we tested mice for cognitive impairment at 1 and 3 months after repeated concussions, using hippocampus-dependent fear conditioning. While WT and control mice exhibited significant impairment in learning and memory, C2CKO mice did not exhibit any significant deficits (Fig. 2, G and H). We also analyzed changes in motor function immediately and for 2 weeks after the last concussion using the beam-walking test, which has previously been used to detect the effects of concussion on speed and balance. Repeated concussions produced a relatively mild impairment, as evidenced by increase in both the time to cross the beam and the number of foot slips at 1 hour, 1 day, and 4 days after the last concussion. WT mice recovered 7 days later (fig. S2, A and B). While C2CKO mice performed a little better than WT, the differences were not statistically significant.

(A and B) Changes in tail suspension task at 1 (A) and 3 (B) months after repeated concussions. Groups of sham and rmTBI WT, C2CKO, and control mice were suspended by the tail for 5 min. The time during which the animals remained immobile was recorded. n = 9 for WT and C2CKO groups, and n = 8 for control groups. Results are means SEM. *P < 0.05. One-way ANOVA followed by Bonferronis test. (C to F) Changes in plus-elevated maze at 1 [(C) and (D)] and 3 [(E) and (F)] months after repeated concussions. Groups of sham and rmTBI WT, C2CKO, and control mice were placed in an elevated plus maze, and the time spent in open arms [(C) and (E)] and number of entries in open arms [(D) and (F)] were recorded. n = 9 for WT and C2CKO groups, and n = 8 for control groups. Results are means SEM. *P < 0.05. One-way ANOVA followed by Bonferronis test. (G and H) Performance in fear conditioning test at 1 (G) and 3 (H) months after repeated concussions. Groups of sham and rmTBI WT, C2CKO, and control mice were trained in the context test of the fear conditioning task. They were tested the following day, and the percent freezing time over 5-min test was recorded. n = 8 for WT and C2CKO groups, and n = 7 for control groups. Results are means SEM. *P < 0.05. One-way ANOVA followed by Bonferronis test.

A major pathological hallmark of repeated concussions is brain inflammation reflected by activation of both astrocytes and microglia (1). We analyzed astrocyte and microglia activation in the brain at 3 months following repeated concussions. We used immunohistochemistry (IHC) to label glial fibrillary acidic protein (GFAP)positive astrocytes (Fig. 3A and fig. S3) and Iba-1positive microglia (Fig. 3C and fig. S4) and quantitatively determined the numbers of reactive astrocytes and activated microglia, as described in Materials and Methods. The numbers of reactive astrocytes and activated microglia were significantly increased in hippocampus and cortex of WT and control mice (Fig. 3, B and D, and figs. S3 and S4). In contrast, C2CKO mice did not exhibit any significant increase in number of reactive astrocytes or activated microglia.

Groups of sham and rmTBI WT, C2CKO, and control mice were sacrificed 3 months after repeated concussions. (A) Changes in astrocyte activation in field CA1 of hippocampus. Brains were fixed and processed for IHC with GFAP antibodies. Scale bar, 100 m. (B) Quantification was performed, as described in Materials and Methods. n = 8 for WT and C2CKO groups, and n = 7 for control groups. ***P < 0.001 and ****P < 0.0001. One-way ANOVA followed by Bonferronis test. Data represent means SEM. (C) Changes in microglia activation in field CA1 of hippocampus. Brains were fixed and processed for IHC with iba-1 antibodies. Scale bar, 100 m. (D) Quantification was performed, as described in Materials and Methods. n = 8 for WT and C2CKO groups, and n = 7 for control groups. *P < 0.05 and ****P < 0.0001. One-way ANOVA followed by Bonferronis test. Data represent means SEM. (E) Changes in axonal degeneration in the optic tract. Brains were fixed and processed for Gallyas staining. Scale bar, 100 m. (F) Quantification was performed, as described in Materials and Methods. n = 6. **P < 0.01. One-way ANOVA followed by Bonferroni test. Data represent means SEM.

Another hallmark of repeated concussions is axonal degeneration in various neuronal tracts (1). We used Gallyas staining to visualize axonal degeneration 3 months after repeated concussions (Fig. 3, E and F). Axonal degeneration was prominent in the optic tract in WT and control mice subjected to repeated concussions. No significant axonal degeneration was observed in C2CKO mice after repeated concussions. Image analysis was used to quantify the results and confirmed the significant axonal degeneration following repeated concussions in WT and control mice and its absence in C2CKO mice. Neuronal loss has also been observed in some models of repeated concussions (29). We therefore determined the number of neurons in various brain structures following repeated concussions in WT mice. Under our experimental conditions, we did not detect a significant decrease in the number of NeuN-positive cells in various brain regions 3 months following repeated concussions in WT mice (fig. S5, A to C).

As mentioned above, one of the hallmarks of CTE is a massive increase in tau hyperphosphorylation at various residues in various brain regions. We had previously observed tau hyperphosphorylation in the CCI mouse model of TBI and proposed the hypothesis that this effect was triggered at least, in part, by calpain-2mediated cleavage of the tyrosine phosphatase, PTPN13, and the resulting activation of c-Abl (22). In the present study, massive increase in tau phosphorylation at threonine 231 was present in cortex, corpus callosum, and optic tract 3 months after rmTBI in WT and control mice (Fig. 4, A to F). On the other hand, no significant changes in tau phosphorylation were detected in C2CKO mice. TDP-43 is an RNA/DNA binding protein, which accumulates in neurons in ALS and FTLD (30). One of the hypotheses for its accumulation in these diseases is that TDP-43 is partially cleaved by calpain, preventing its nuclear transport and inducing its cytosol accumulation and aggregation (31). We therefore determined changes in cortical levels of TDP-43 following rmTBI in WT and C2CKO mice at 1, 3, and 7 days after repeated concussions (Fig. 1, C and E). TDP-43 levels were significantly decreased at these three time points in WT mice but were unchanged in C2CKO mice. In cortex, phosphoTDP-43 (p-TDP-43), the pathological form of TDP-43, exhibited changes in subcellular localization, with accumulation in the cytoplasm and decreased expression in the nucleus, where it is found under control conditions (Fig. 4, G and H), which were very similar to what has been reported in human patients with ALS or FTLD (30). These changes in p-TDP-43 localization were completely absent in C2CKO mice (Fig. 4, G and H).

Groups of sham and rmTBI WT, C2CKO, and control mice were sacrificed 3 months after repeated concussions. (A, C, and E) Changes in tau phosphorylation in cortex, corpus callosum, and optic tract. Brains were fixed and processed for IHC with phospho-tau (p-tau) Thr231 antibodies. Scale bars, 20 m. (B, D, and F) Quantification of images similar to those shown. n = 6 for WT sham; n = 7 for C2CKO sham, control sham, and control rmTBI; n = 8 for WT rmTBI and C2CKO rmTBI. *P < 0.05, **P < 0.01, and ***P < 0.001. One-way ANOVA followed by Bonferronis test. Data represent means SEM. (G) Changes in phosphoTDP-43 (p-TDP-43) subcellular localization in cortex. Brains were fixed and processed for IHC with a p-TDP-43 Ser409/Ser410 antibody. Scale bar, 20 m. (H) Quantification of the p-TDP-43 intensity ratio of nuclei to cytoplasm. n = 4. ***P < 0.001 and ****P < 0.0001. One-way ANOVA followed by Bonferronis test. Data represent means SEM.

We previously identified a relatively selective calpain-2 inhibitor, C2I (32), which provides a significant degree of protection against pathological changes in the CCI mouse model of TBI, when injected intraperitoneally after TBI (22). For the present study, in which repeated concussions were administered over a period of 10 days, we selected to deliver C2I through subcutaneously implanted Alzet minipumps. We first verified that this mode of delivery was effective to inhibit calpain-2mediated neurodegeneration in cortex in the CCI model (fig. S5, D and E). The pumps were then implanted the day before the start of the concussions and were withdrawn after 2 weeks. Animals were tested for motor impairment immediately at the end of the repeated concussions and for cognitive impairment 1 month later. They were then sacrificed, and the same pathological markers used previously were analyzed. Animals treated with C2I were significantly protected against the depression symptom (fig. S6A), the risk-taking behavior (fig. S6, B and C), and cognitive impairment, assessed with novel object location (fig. S6D) and hippocampus-dependent fear conditioning (fig. S6E). These results were quite similar to those observed in the C2CKO mice, although the animals were tested 1 month after the last concussion. We also analyzed changes in motor function immediately and for 2 weeks following the last concussion using the beam-walking test (fig. S2, C and D). The results in animals treated with C2I were very similar to those we observed in C2CKO mice; and although C2I-treated animals performed slightly better than vehicle-treated animals, the differences were not statistically significant. Astrogliosis, microglial activation, and axonal degeneration were analyzed 1 month after the last concussion (Fig. 5). Animals treated with C2I did not exhibit significant astroglial (Fig. 5, A and B) and microglial (Fig. 5, C and D) activation in field CA1; they also did not show astroglial or microglial activation in CA3, dentate gyrus, or cortex (figs. S7 and S8). Axonal degeneration 1 month after concussion was observed in the optic tract (Fig. 5, E and F) in vehicle-treated animals but was not significantly changed in animals treated with C2I. We also observed axonal degeneration in cortex and in corpus callosum 1 month after the last concussion in vehicle-treated animals, and this effect was much reduced by C2I treatment (fig. S9). One month after the last concussion increased tau phosphorylation was observed in various brain regions in vehicle-treated animals, including cortex (Fig. 6, A and B), corpus callosum (Fig. 6, C and D), and optic tract (Fig. 6, E and F). These changes in tau phosphorylation were absent in animals treated with C2I. Changes in p-TDP-43 subcellular localization were also observed 1 month after the last concussion in cortex, with p-TDP-43 being almost exclusively translocated from the nucleus to the cytoplasm (fig. S10, A and B). TDP-43 subcellular localization was not significantly altered in C2I-treated mice. Last, levels of p-TDP-43 were significantly increased after rmTBI in the optic tract (fig. S10, C and D), suggesting abnormal processing of p-TDP-43 in the axons of retinal ganglion cells. Levels of p-TDP-43 in the optic tract were not significantly increased after rmTBI in C2I-treated mice.

WT mice were implanted with Alzet minipumps delivering vehicle [veh; 400 mg/ml; (2-hydroxypropyl)--cyclodextrin] or C2I (0.3 mg kg1 day1) 1 day before 10 days of repeated concussions. Pumps were withdrawn 4 days after the last day of concussion, and the animals were sacrificed 4 weeks later. (A) Changes in astrocyte activation in field CA1 of hippocampus. Brains were fixed and processed for IHC with GFAP antibodies. Scale bar, 100 m. (B) Quantification of images similar to those shown. n = 8 for veh sham and veh rmTBI, n = 7 for C2I sham, n = 9 for C2I rmTBI. **P < 0.01. One-way ANOVA followed by Bonferronis test. Data represent means SEM. (C) Changes in microglia activation in field CA1 of hippocampus. Brains were fixed and processed for IHC with iba-1 antibodies. Scale bar, 100 m. (D) Quantification of images similar to those shown. n = 8 for veh sham and veh rmTBI; n = 7 for C2I sham; and n = 9 for C2I rmTBI. *P < 0.05. One-way ANOVA followed by Bonferronis test. Data represent means SEM. (E) Changes in axonal degeneration in the optic tract. Brains were fixed and processed for Gallyas staining. Scale bar, 100 m. (F) Quantification of images similar to those shown. n = 6. **P < 0.01. One-way ANOVA followed by Bonferronis test. Data represent means SEM.

WT mice were implanted with Alzet minipumps delivering vehicle [400 mg/ml; (2-hydroxypropyl)--cyclodextrin] or C2I (0.3 mg kg1 day1) 1 day before 10 days of repeated concussions. Pumps were withdrawn 4 days after the last day of concussion, and the animals were sacrificed 4 weeks later. (A, C, and E) Changes in tau phosphorylation in cortex, corpus callosum, and optic tract. Brains were fixed and processed for IHC with p-tau Thr231 antibodies. Scale bars, 20 m. (B, D, and F) Quantification of images similar to those shown. n = 8 for veh sham and veh rmTBI; n = 7 for C2I sham; and n = 9 for C2I rmTBI. *P < 0.05, **P < 0.01, and ***P < 0.001. One-way ANOVA followed by Bonferronis test. Data represent means SEM.

Our results demonstrate that calpain-2 activation plays a critical role in the development of neuropathology following repeated concussions. Thus, both the functional impairment and the pathological manifestations of brain damage, including inflammation, axonal degeneration, and tau and TDP-43 abnormalities, were absent in mice with genetic calpain-2 deletion or treatment with a relatively selective calpain-2 inhibitor. One of the difficulties to identify novel therapeutic treatments for neurological diseases has been the lack of reproducibility in the animal models used in various laboratories. It is therefore reassuring that our results in the mouse model of repeated mild concussions are in excellent agreement with the findings reported by Petraglia et al. (25, 26) and others (1). Thus, we observed early impairment in motor function, which rapidly recovered, and changes in depression symptoms and risk-taking behavior similar to those previously reported. While previous studies have used the Morris water maze to analyze changes in cognitive behavior, we used fear conditioning as an index of cognition and also observed changes in performance in this paradigm, confirming that rmTBI results in impaired cognition. We observed widespread astroglia and microglia activation at 1 and 3 months after the last concussion. We identified reactive astrocytes on the basis of their larger size and number of processes (33) and quantified their numbers in various brain regions. Our results demonstrated increased numbers of reactive astrocytes at 1 and 3 months after repeated concussions. In contrast, there was no increase in the numbers of reactive astrocytes in C2CKO mice or after treatment with the selective calpain-2 inhibitor. Similarly, we identified reactive microglia on the basis of larger and irregular soma (34) and quantified their numbers in various brain regions after repeated concussions. Our results indicated that there was a significant increase in the numbers of reactive microglia after repeated concussions in WT and control mice but no increase following down-regulation of calpain-2 or pharmacological inhibition. Increased tau phosphorylation was present in various brain regions, as previously reported in various models of mTBI (35). Axonal degeneration was present in corpus callosum and optic tract, in good agreement with previous reports (26). While some neuronal degeneration has been reported in some model of repeated concussions (29), we did not observe any significant neuronal loss 3 months after repeated concussions in WT mice. It is conceivable that Wallerian degeneration could take place and that neuronal loss could develop more slowly in the model we used. We also confirmed that, in this model, alterations in TDP-43, which had been previously reported in ALS and frontotemporal dementia (30), were also present in cortex. Thus, TDP-43 levels in cortex were decreased up to 7 days after repeated concussions in WT but not in C2CKO. In addition, TDP-43 exhibited changes in subcellular localization from the nucleus in control animals to the cytoplasm 3 months after repeated concussions. This change in subcellular localization has been previously discussed in relationship to calpain-mediated cleavage, leading to aggregation in the cytoplasm and contributing to the neurodegeneration observed in these disorders (35). Our findings strongly suggest that following rmTBI, TDP-43 could also be cleaved by calpain-2 and localized to the cytoplasm where aggregated TDP-43 could contribute to neurodegenerative changes. Several studies have shown that TBI can lead to CTE and ALS (3), although the potential mechanisms underlying the development of either CTE or ALS following TBI or repeated concussions are not well understood (36).

Although calpain has been repeatedly proposed to play a significant role in TBI (10, 11), there are only few data regarding the respective roles of calpain-1 and calpain-2, two of the major calpain isoforms, in TBI or concussion. We previously reported that, while calpain-1 was rapidly and transiently activated in a mouse model of TBI, calpain-2 activation was delayed and prolonged (22). Comparing the changes in SBDP in cortex and hippocampus between WT and C2CKO mice, our results indicate that in the rmTBI model, calpain-2 is activated 24 hours after the last concussion and remains activated for up to 1 week in both cortex and hippocampus. This time course of calpain-2 activation is quite similar to what we observed in the more severe TBI model we previously used. In the TBI model, we also observed that levels of calpain-2 activation were closely related to the extent of degenerating cells. In the less severe model of repeated concussions, there was no clear evidence of degenerating cells, as previously reported, suggesting that the extent of calpain-2 activation might not be sufficient to trigger cell death.

While the extent of calpain-2 activation might not have been sufficient to trigger significant cell death, it was sufficient to trigger a whole host of neurodegenerative events, including activation of astrocytes and microglia and axonal degeneration in several tracts, such as in the corpus callosum and the optic tract, since all these events were lacking in calpain-2 KO mice. These results are somewhat different from what we observed in the TBI model. In this model, we did observe massive astroglial activation 7 days after TBI in the cortex surrounding the lesion, and this was not blocked by a daily injection with a selective calpain-2 inhibitor (22). In the present study, continuous administration of the same calpain-2 inhibitor prevented glial reaction and axonal degeneration observed at 1 month after the last concussion. Reasons for this difference are currently not clear. It could be that genetic calpain-2 deletion or continuous administration of the calpain-2 inhibitor provides better calpain-2 inhibition than the daily intraperitoneal injections. It could also be related to the differences in time points selected in the two studies, since we analyzed glial activation at 1 month after concussion and not 1 week. In any event, glial activation is generally considered to have a dual effect in neurodegeneration, depending on the types of glial cells activated (37). In our studies, we did not attempt to distinguish between different subtypes of astrocytes or microglia, but it is quite remarkable that calpain-2 deletion completely eliminated both astrocyte and microglia activation. As previously mentioned, TBI and rmTBI have been shown to be associated with increased tau phosphorylation at various sites. We previously reported an increased tau phosphorylation at residue Tyr245 in the CCI model of TBI, and this effect was significantly reduced following treatment with C2I (38). In the present study, we also found that calpain-2 deletion in excitatory neurons from the forebrain completely prevented rmTBI-induced increased in tau phosphorylation. We previously proposed that calpain-2mediated truncation of the tyrosine phosphatase, PTPN13, represents a link between calpain-2 and tau phosphorylation, as one of the targets of PTPN13 is c-Abl, which can phosphorylate tau at Tyr245. However, there are other pathways that could be regulated by calpain, including glycogen synthase kinase (39), which can also result in tau phosphorylation at various residues.

We used a relatively selective calpain-2 inhibitor, Z-Leu-Abu-CONH-CH2-C6H3 (C2I), to further confirm the role of calpain-2 in rmTBI-mediated behavioral impairments and neuropathology. Because of the duration of the repeated concussions and the prolonged activation of calpain-2 in this model, we selected to continuously deliver C2I through subcutaneously implanted minipumps, which significantly prevented calpain-2 activation in the brain following trauma. Treatment of WT mice with C2I reproduced all the beneficial effects of calpain-2 deletion at the behavioral and neuropathological levels. Thus, C2I-treated mice did not exhibit the depression symptom or the risk-taking behavior of the vehicle-treated mice. They also did not exhibit the cognitive impairment in the fear conditioning task. Activation of astrocytes and microglia was also almost completely prevented in the different brain regions tested. Likewise, increased tau phosphorylation and changes in subcellular localization of TDP-43 were almost completely blocked by C2I treatment.

Our results establish that calpain-2 activation is a critical step, leading to a wide range of neuropathological changes and behavioral alterations following repeated concussions. They also demonstrate that treatment with a selective calpain-2 inhibitor represents a novel potential therapeutic approach to prevent brain damage and behavioral modifications following repeated concussions. In the present experiments, we started treatment with the selective calpain-2 inhibitor the day before the first concussion episode, and our results suggest the possibility of using a similar approach for individuals at risk for CTE, such as athletes in sport contact and military personnel. Future experiments will be directed at determining the effects of posttreatment with the inhibitor to further establish the possibility of using this treatment in human participants exposed to concussion. Considering that a blood biomarker based on calpain activation has been proposed to be a predictive diagnostic tool for human concussion, and that tau PET has recently been shown to be a useful tool to investigate neurodegeneration after TBI in human participants (40), our results further warrant pursuing the development of a selective calpain-2 inhibitor for the treatment of concussions.

The objective of this study is to examine the role of calpain-2 in the pathology of repetitive mTBI. For this, we performed rmTBI or sham procedure on three groups of mice. The first group consisted of 16 WT mice and 16 C2CKO mice. Mice were euthanized at 1, 3, and 7 days after rmTBI (four mice for each time point) or 1 day after sham procedure. Brain tissue was collected to analyze markers for calpain activation, SBDP, and for early pathological tau, PAD-tau. The second group of mice consisted of WT mice, C2CKO mice, and calpain-2 loxP mice (control for calpain-2 CKO). There were ~18 mice for each genotype (half for rmTBI and half for sham). Beam-walking tests were performed from 0 to 14 days after rmTBI. Elevated plus maze, tail suspension, and fear conditioning tests were performed at 1 and 3 months after rmTBI. The third group of mice consisted of WT mice treated with C2I or vehicle. There were ~18 mice for C2I and ~18 mice for vehicle. Beam-walking tests were performed from 0 to 14 days after rmTBI. Elevated plus maze, tail suspension, novel object, and fear conditioning tests were sequentially performed at 1 month after rmTBI. For the second and third group, mice were euthanized after behavioral tests and IHC was performed on brain sections to examine several pathological markers such as GFAP, iba-1, phospho-tau (p-tau), and p-TDP-43. Silver staining was also performed to examine neurodegeneration. In rare cases, mice showing abnormalities such as signs of pain, motor impairment, and seizures during rmTBI procedure were immediately removed from the study. Specifically, one mouse was removed from the WT rmTBI group, two mice were removed from the control rmTBI group, one mouse was removed from the vehicle rmTBI group, while no mouse was removed from the C2CKO rmTBI or C2I rmTBI group. For all behavioral and IHC studies, experiments and data analysis were done by two persons in a blind fashion.

Animal experiments were conducted in accordance with the principles and procedures of the National Institutes of Health Guide for the Care and Use of Laboratory Animals. All protocols were approved by the local Institutional Animal Care and Use Committee.

We used C57Bl/6 (WT), CamKII-Cre+/ CAPN2loxP/loxP (calpain-2 CKO), and CAPN2loxP/loxP (loxPcalpain-2) mice, referred to as control. All mice are on a C57Bl/6 background.

Primary antibodies for Western blot: SBDP (1:20; MAB1622, EMD Millipore) and PAD-tau (1:20; MABN417, EMD Millipore). Primary antibodies for IHC: calpain-1 (1:200; LS-B4768, LSBio), calpain-2 (1:300; LS-C337641, LSBio), GFAP (1:1000; AB5804, Abcam), iba-1 (1:400; AB5076, Abcam), p-tau Thr231 (1:200; MN1040, Thermo Fisher Scientific), p-TDP-43 409/410 (1:400; 22309-1-AP, Proteintech), and NeuN (1:200; ab104224, Abcam). Secondary antibodies for IHC: Alexa Fluor 594 goat anti-rabbit immunoglobulin G (IgG) (1:400; A11037, Thermo Fisher Scientific), Alexa Fluor 594 goat anti-mouse IgG (1:400; A11005, Thermo Fisher Scientific), and Alexa Fluor 594 donkey anti-goat IgG (1:400; A11058, Thermo Fisher Scientific).

NMDA toxicity in acute hippocampal slices from postnatal days 14 to 16 WT or C2CKO mice was analyzed, as previously described (23). Mice at postnatal days 14 to 16 were anesthetized with halothane and decapitated. Brains were quickly removed and transferred to oxygenated, ice-cold cutting medium: 124 mM NaCl, 26 mM NaHCO3, 10 mM glucose, 3 mM KCl, 1.25 mM KH2PO4, 5 mM MgSO4, and 3.4 mM CaCl2. Hippocampal transversal slices (400 m thick) were prepared using a McIlwain-type tissue chopper and transferred to a recovery chamber with a modified artificial cerebrospinal fluid medium, containing: 124 mM NaCl, 2.5 mM KCl, 2.5 mM CaCl2, 1.5 mM MgSO4, 1.25 mM NaH2PO4, 24 mM NaHCO3, 10 mM d-glucose, and saturated with 95% O2/5% CO2 for 1 hour at 37C. Slices were then treated with NMDA (100 M) for 3 hours. At the end of treatment, 50 l of medium solution was transferred to a 96-well plate, and the LDH reaction was performed using the Pierce LDH Cytotoxicity Assay Kit (Thermo Fisher Scientific) following the manufacturers instruction. To determine LDH activity, the absorbance at 680 nm (background signal) was subtracted from the absorbance at 490 nm. LDH activity was normalized to protein concentration, and results are shown as fold of controls.

The rmTBI model was established in mice following the protocol described in a previous publication (25), with minor changes. Briefly, mice were restrained in a plastic restraint cone (89066-338, VWR International) without anesthesia and placed on a foam bed. The mouse head was not immobilized. This setting better mimics the human concussive injury, which often happens under awake conditions and the head undergoes acceleration and deceleration. A stainless steel helmet (6 mm diameter) (Millenium Machinery, Rochester, NY) was placed on the right hemisphere between the lambda and bregma. A 1.0-mm-thick double-sided gel tape (Scotch) was stick to the underside of the helmet. A pneumatically controlled impactor device (AMS-201, Amscien) was modified to deliver mild closed-head impacts. The impactor tip was replaced with a rubber round tip (6 mm diameter) to reduce the incidence of skull fracture. The impact depth was 5 mm. The impact speed was 3.5 m/s. The duration of impact was 100 ms. The impact angle was 20 from the vertical plane. After impact, mice were removed from the restraint bag and returned to their cage. Mice showing abnormalities, such as signs of pain, motor impairment, or seizures, were rarely seen and were removed from the study. Animals received four head impacts per day with a 2-hour interval between impacts for 10 days. Sham groups underwent the same procedure as the rmTBI groups. They were placed into the restraint cone on the same foam bed. However, no impacts were given.

Osmotic pumps (Model 2002, ALZET; release rate, 0.5 l/hour) were filled with 200 l of C2I (0.625 g/l) in (2-hydroxypropyl)--cyclodextrin (400 mg/ml) or with 200 l of (2-hydroxypropyl)--cyclodextrin (400 mg/ml) as vehicle. Pumps were implanted subcutaneously in mice 1 day before rmTBI and removed 4 days after the last episode of rmTBI (total of 15 days). Approximately, 0.3 mg/kg of C2I was released per day. This dose is the same as the daily dose used for intraperitoneal injections of C2I in a mouse model of TBI (22).

At indicated time points after rmTBI, ipsilateral cortical and hippocampal tissues were collected from WT and C2CKO mice. Tissues were homogenized in lysis buffer (87787, Thermo Fisher Scientific), containing protease and phosphatase inhibitor cocktails (78446, Thermo Fisher Scientific), and protein concentration was measured with the bicinchoninic acid (BCA) assay (23225, Thermo Fisher Scientific). Western blot was done using the Wes system (ProteinSimple): 1.2 g of total protein of samples was loaded to each lane and 12 to 230 kDa separation modules were used. For the detection of PAD-tau, samples were run under nonreducing conditions. Peak areas of the bands were measured by Compass software (ProteinSimple).

At 1 or 3 months after rmTBI, mice were anesthetized and intracardially perfused with 0.1 M phosphate buffer (pH 7.4) and then with freshly prepared 4% paraformaldehyde in 0.1 M phosphate buffer. Brains were removed and immersed in 4% paraformaldehyde at 4C for 1 day for postfixation and then in 15 and 30% sucrose at 4C for 1 day each for cryoprotection. Coronal frozen sections (20 m thick) at bregma 1.58 to 2.30 in each brain were collected. Two sections (at 160-m interval) per animal were evaluated for each specific immunohistochemical analysis. Sections were first blocked in 0.1 M phosphate-buffered saline (PBS) containing 5% goat or donkey serum and 0.3% Triton X-100 (blocking solution) for 1 hour and then incubated with primary antibody prepared in blocking solution overnight at 4C. Sections were washed three times in PBS and incubated in Alexa Fluor secondary antibody prepared in blocking solution (1:400) for 2 hours at room temperature. After three washes, sections were mounted with mounting medium containing 4,6-diamidino-2-phenylindole (Vector Laboratories). Sections were visualized under confocal microscopy (ZEISS LSM 880). Imaging parameters were constant within each specific antigen analysis. For the quantification of reactive astrocytes, 332 m by 332 m areas from indicated brain regions were analyzed in each GFAP-labeled section. Image threshold was adjusted to highlight astrocytes processes. Astrocytes with 4 processes visible 30 m from the soma were considered as reactive astrocytes and were manually counted in each image. For the quantification of reactive microglia, 332 m by 332 m areas from indicated brain regions of each iba-1labeled section were analyzed. Image threshold was adjusted to highlight microglia soma. Microglia with soma size 28 m2 and circularity 0.6 were considered as reactive microglia and were counted using the Analyze Particles function of ImageJ. For the quantification of p-tau signals, 135 m by 135 m areas from indicated brain regions of each section were analyzed. The thresholded area of each image was measured using ImageJ. For the quantification of p-TDP-43 translocation, 135 m by 135 m areas from indicated brain regions of each section were analyzed. The ratio of the intensity in nuclei to the intensity in cytoplasm was calculated using an ImageJ macro named Intensity Ratio Nuclei Cytoplasm Tool. For the quantification of NeuN-positive cells, 664 m by 249 m areas in the lateral geniculate nucleus and parietal cortex and 166 m by 58 m areas in hippocampal CA1, CA3, and dentate gyrus (DG) were analyzed. Image threshold was adjusted, and NeuN-positive nuclei were counted using the Analyze Particles function of ImageJ. Image acquisition and quantification were done by two persons in a blind fashion.

Coronal frozen sections (40 m thick) at bregma 2.30 in each brain were collected. Gallyas silver staining was performed using the FD NeuroSilver Kit II (FD NeuroTechnologies). Areas (444 m by 321 m) at indicated brain regions of each section were imaged under a light microscope (Zeiss Axiophot). The thresholded area of each image was measured using ImageJ. Image acquisition and quantification were done by two persons in a blind fashion.

TUNEL (terminal deoxynucleotidyl transferasemediated deoxyuridine triphosphate nick end labeling) staining was performed in a set of coronal frozen sections (20 m thick) at bregma 0.50, 0.58, and 1.58 mm using the ApopTag in situ apoptosis detection kit (S7165, Millipore). Sections were visualized under confocal microscopy (LSM 880, Zeiss). All TUNEL-positive nuclei surrounding the lesion area in the sections were counted using the analyze particles function in ImageJ. Total number of TUNEL-positive nuclei in a set of sections of each brain was summed. Image acquisition and quantification were done by two persons in a blind fashion.

The beam apparatus consists of a 1-m wooden round beam with a diameter of 2 cm, resting 50 cm above the tabletop on two poles. A black box is placed at the end of the beam as the finish point. Nesting material from home cages is placed in the black box to attract the mouse to the finish point. A lamp (with 60-W light bulb) is used to shine light above the start point and serves as an aversive stimulus. Each mouse is placed on a brightly lit platform and is allowed to transverse the round beam. A nylon hammock is stretched below the beam, about 7.5 cm above the tabletop, to cushion any falls. On training day, mice are allowed to cross the beam, with gentle guiding or prodding as needed, until they cross readily. The timer is started by the nose of the mouse entering the start point and stopped when the animal reaches the safe box. Mice rest for 10 min in their home cages between training sessions. Mice are trained three times. The beams and box are cleaned of mouse droppings and wiped with towels soaked with 70% ethanol and then water before the next mouse is placed on the apparatus. On testing day, mice are placed on the beam, and numbers of back paw slips and latency to cross are scored. Mice are tested three times with 10-min interval for resting. Results for the three tests are averaged to provide individual values for each mouse on that day. The experiments were performed and results analyzed by a blind observer.

Elevated plus maze for mice was performed following the protocol described in a previous publication (41). Briefly, the maze is painted black and consists of two open arms without walls and two closed arms with 15-cm-high walls. Each arm is 30 cm long and 5 cm wide. The maze is elevated 40 cm off of the floor. Mice were transferred to the behavioral testing room in their home cage 1 hour before the test. At the beginning of the test, mouse was placed at the center of the plus maze, facing an open arm opposite to the location of the operator. The movement of the mouse was recorded by a camera at the top of the maze for 5 min. The mouse was then returned to its home cage. The maze was cleaned with disinfectant and dried with paper towels before testing the next mouse. Video was later analyzed manually. Open-arm time, closed-arm time, open-arm entries, and closed-arm entries were counted. An arm entry was counted when all four paws of the mouse were in that arm. Behavioral test and video analysis were done by two persons in a blind fashion.

The tail suspension test was performed following the protocol described in a previous publication (42). Briefly, the tail suspension box was made of wood and painted white. It is 55 cm high, 60 cm wide, and 11.5 cm deep. It has four compartments to test four mice at a time. A suspension bar (1 cm high, 1 cm wide, and 60 cm long) was positioned on the top of the box. Mice were transferred to the behavioral testing room in their home cage 1 hour before the test. A 17-cm-long tape was attached to the end of the mouse tail. The mice were suspended in each compartment by placing the free end of the tape on the suspension bar. The movement of the mice was recorded for 6 min by a camera in front of the tail suspension box. The mice were then returned to their home cage, and the tape was gently removed from the tail. The box was wiped with disinfectant before the next round of test. Video was later analyzed by another observer. The time that each mouse spends as mobile was measured, following the criteria described in (39). The immobility time was then calculated as total time minus mobility time. Behavioral test and video analysis were done by two persons in a blind fashion.

For fear conditioning, we used the same protocol we used in our previous studies (22). On training day, mice were placed in the fear conditioning chamber (H1011M-TC, Coulbourn Instruments) located in the center of a sound-attenuating cubicle (Coulbourn Instruments). After a 2-min exploration period, one tonefoot shock pairings separated by 1-min intervals were delivered. The 85-dB, 2-kHz tone lasted for 30 s, and the foot shock was 0.75 mA and lasted for 2 s. Foot shock coterminated with the tone. Mice remained in the training chamber for another 30 s before being returned to their home cages. Context test was performed 1 day after training. On day 3, animals were subjected to a cue/tone test. The same conditioning chamber was modified by changing its metal grid floor to a plastic sheet, white metal walls to plastic walls gridded with red tapes, and odor from ethanol to acetic acid. Mice were placed in the altered chamber for 5 min to measure freezing level in the altered context; and after this 5-min period, a tone (85 dB, 2 kHz) was delivered for 1 min to measure freezing to tone. Mice behavior was recorded with the FreezeFrame software and analyzed with FreezeView software (Coulbourn Instruments). Motionless bouts lasting 1 s were considered as freezing. The percentage of time animal froze was calculated, and the group means with SEM and accumulative distribution of percentage freeze were analyzed.

Novel object location tests were performed, as previously described (43). Before training, mice habituated to the experimental apparatus for 5 min in the absence of objects. During habituation, animals were allowed to explore an empty arena. Twenty-four hours after habituation, animals were exposed to the familiar arena, with two identical objects added and allowed to explore for 10 min. During the retention test, mice were allowed to explore the experimental apparatus for 6 min. Exploration was scored when a mouses head was oriented toward the object within a distance of 1 cm or when the nose was touching the object. The relative exploration time was recorded and expressed as a discrimination index [DI = (tnovel tfamiliar)/(tnovel + tfamiliar) 100%]. Mean exploration times were then calculated, and the discrimination indexes between treatment groups were compared. Mice that explored both objects for 3 s in total during either training or testing were removed from further analysis. Mice that demonstrated an object preference during training (DI >20) were also removed.

E. B. Cagmat, J. D. Guingab-Cagmat, A. V. Vakulenko, R. L. Hayes, J. Anagli, Potential Use of Calpain Inhibitors as Brain Injury Therapy. in Brain Neurotrauma: Molecular, Neuropsychological and Rehabilitation Aspects, F. H. Kobeissy, Ed. (CRC Press/Taylor & Francis, 2015), Chapter 40.

Acknowledgments: Funding: This work was supported by the Office of the Assistant Secretary of Defense for Health Affairs through The Defense Medical Research and Development Program under Award no. W81XWH-19-1-0329. Opinions, interpretations, conclusions, and recommendations are those of the author and are not necessarily endorsed by the U.S. Department of Defense. Grant no. BA170606. Optimization of a selective calpain-2 inhibitor for prolonged field care in traumatic brain injury. X.B. is supported, in part, by funds from the Daljit and Elaine Sarkaria Chair. Author contributions: Y.W., X.B., and M.B. designed the experiments, analyzed the data, and wrote the manuscript. Y.W., Y.L., A.N., A.S., D.Q., E.Y., and D.R. provided experimental data and analyzed data. Competing interests: M.B., X.B., and Y.W. are cofounders of NeurAegis, a startup company focusing on developing selective calpain-2 inhibitors for the treatment of acute neurodegeneration. M.B. is an inventor on a Provisional Patent New selective calpain-2 inhibitors for the treatment of neurodegeneration. The other authors declare no competing interests. Data and materials availability: All data needed to evaluate the conclusions in the paper are present in the paper and/or the Supplementary Materials. Additional data related to this paper may be requested from the authors.

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Calpain-2 as a therapeutic target in repeated concussioninduced neuropathy and behavioral impairment - Science Advances

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Prospective randomized trial of interventions for vincristine-related neuropathic pain. – Physician’s Weekly

Monday, July 6th, 2020

To evaluate the efficacy of gabapentin at 20mg/kg per day in the treatment of vincristine-related neuropathic pain.Children aged 1-18years who developed vincristine-induced neuropathy on a St Jude frontline acute lymphoblastic leukemia trial were prospectively enrolled on a randomized, double-blind, placebo-controlled, phase II trial with two treatment arms: gabapentin plus opioid versus placebo plus opioid. Daily evaluations of morphine dose (mg/kg per day) and pain scores were conducted for up to 21days; the values of the two arms were compared to assess analgesic efficacy.Of 51 study participants, 49 were eligible for analyses. Twenty-five participants were treated with gabapentin, with a mean (SD) dose of 17.97 (2.76) mg/kg per day (median 18.26, range 6.82-21.37). The mean (SD) opioid doses taken, expressed as morphine equivalent daily (mg/kg per day), were 0.26 (0.43) in the gabapentin group (25 patients, 432days) and 0.15 (0.22) in the placebo group (24 patients, 411days; P=.15). Only the risk classification of acute lymphoblastic leukemia was significantly associated with the daily morphine dosage (P=.0178): patients in the lower risk arm received higher daily morphine dosages. Multivariate analyses revealed a significant difference between the groups average daily scores for the previous 24h and right now.In this population of children with vincristine-related neuropathic pain, opioid consumption and pain scores were higher in the gabapentin group than in the placebo group. Future randomized, double-blind, placebo-controlled studies should test gabapentin given longer or at a higher dose. 2020 Wiley Periodicals LLC.

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Prospective randomized trial of interventions for vincristine-related neuropathic pain. - Physician's Weekly

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Save your feet from diabetic neuropathy: A few tips to keep your feet healthy – TheHealthSite

Monday, June 29th, 2020

Diabetes has assumed epidemic proportions today and millions of people suffer from this condition globally. There may be many causes behind this problem like family history, unhealthy diet and a sedentary lifestyle. Some environmental pollutants may also trigger this condition. It often brings with it many complications like blurry vision, weight loss and excessive thirst. Uncontrolled blood sugar levels over time can result in serious health issues like kidney problems and diabetic retinopathy. Also Read - Diabetes increases your risk of cancer: Experts blame DNA damage

If you have diabetes, you need to take good care of your feet. This is because one of the complications of this condition is diabetic neuropathy. It leads to loss of sensation in your feet and you may be unaware if you have any injury. This happens because fluctuation in blood sugar levels may damage the nerves and vessels of the feet. Unattended injuries can cause gangrene and it may result in loss of a limb. In fact, diabetic neuropathy is the leading cause of amputations in people with diabetes. Also Read - Know how to deal with wounds if you have diabetes

This complication of diabetes may develop over time and you may not notice it immediately. Some people experience a feeling of thickness on their soles. At times, you may also develop open sores and calluses on your soles. If you have an injury, it will take a longer time to heal. A burning sensation on the feet and extreme sensitivity may also be symptoms of diabetic neuropathy. Also Read - Diabetes alert: Beware of dementia and cancer if you have elevated blood sugar levels

If you have this condition, you must be extra careful when it comes to your feet. If you notice any changes in the shape of your feet or any injury that is not healing, seek immediate medical help. This will help you save your feet. One important thing that you need to do is wear the right shoes. There are now many shoes that are especially designed for people with diabetes. These special shoes are deeper than normal shoes. Choose something that is comfortable and fits you well. Make sure that you can wriggle your toes around after wearing your shoes. Avoid wearing heels and fancy open-toed ones. Straps are bad too as it may sometimes cut into your skin and injure you.

Tip: Shop for footwear at the end of the day when your feet may be slightly swollen. This will help you pick a pair that will not be tight around this time of the day.

You can also ask your doctor about wearing compression socks to stimulate circulation in your lower limbs. Other than this, be gentle with your feet and treat them with love and care. Every night before going to bed, make it a point to check your feet properly for any sings of injury. If you notice anything different, get an appointment with your doctor. Be sure to keep your nails trimmed and groomed. You may also give yourself a regular pedicure and use scrubs to exfoliate your feet at frequent intervals. Be sure to wash your feet with warm water before going to bed every night. This night time ritual will go a long way in keeping your feet safe.

Published : June 29, 2020 7:08 pm

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Global Neuropathy Pain Treatment Market 2020 Overview with (Covid-19) Impact Analysis of Growth, Competitive landscape and Forecast 2025 – Bandera…

Monday, June 29th, 2020

The recent research report titledGlobalNeuropathy Pain TreatmentMarket Report 2020, Forecast to 2025sheds light on critical aspects of the market by compiling the historical, current, and future outlook of the market and the factors responsible for such growth. The report contains numerical data and certified data, which is gathered from certified sources and market experts. The document offers useful guidelines for players to understand and define their strategies more efficiently in order to assist them to stay ahead of their competitors. The report includes and evaluates all the changes and shifts that are observed in the globalNeuropathy Pain Treatmentmarket. It encompasses data that is derived from historical trends and present market scenarios.

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Global Neuropathy Pain Treatment Market 2020 Overview with (Covid-19) Impact Analysis of Growth, Competitive landscape and Forecast 2025 - Bandera...

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