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(−)‐Phenserine tartrate (PhenT) as a treatment for traumatic brain injury

Aim Traumatic brain injury (TBI) is one of the most common causes of morbidity and mortality of both young adults and the elderly, and is a key contributing factor in about 30% of all injury‐associated deaths occurring within the United States of America. Albeit substantial impact has been made to i...

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Published in:CNS neuroscience & therapeutics 2020-06, Vol.26 (6), p.636-649
Main Authors: Greig, Nigel H., Lecca, Daniela, Hsueh, Shih‐Chang, Nogueras‐Ortiz, Carlos, Kapogiannis, Dimitrios, Tweedie, David, Glotfelty, Elliot J., Becker, Robert E., Chiang, Yung‐Hsiao, Hoffer, Barry J.
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creator Greig, Nigel H.
Lecca, Daniela
Hsueh, Shih‐Chang
Nogueras‐Ortiz, Carlos
Kapogiannis, Dimitrios
Tweedie, David
Glotfelty, Elliot J.
Becker, Robert E.
Chiang, Yung‐Hsiao
Hoffer, Barry J.
description Aim Traumatic brain injury (TBI) is one of the most common causes of morbidity and mortality of both young adults and the elderly, and is a key contributing factor in about 30% of all injury‐associated deaths occurring within the United States of America. Albeit substantial impact has been made to improve our comprehension of the mechanisms that underpin the primary and secondary injury stages initiated by a TBI incident, this knowledge has yet to successfully translate into the development of an effective TBI pharmacological treatment. Developing consent suggests that a TBI can concomitantly trigger multiple TBI‐linked cascades that then progress in parallel and, if correct, the multifactorial nature of TBI would make the discovery of a single effective mechanism‐targeted drug unlikely. Discussion We review recent data indicating that the small molecular weight drug (−)‐phenserine tartrate (PhenT), originally developed for Alzheimer's disease (AD), effectively inhibits a broad range of mechanisms pertinent to mild (m) and moderate (mod)TBI, which in combination underpin the ensuing cognitive and motor impairments. In cellular and animal models at clinically translatable doses, PhenT mitigated mTBI‐ and modTBI‐induced programmed neuronal cell death (PNCD), oxidative stress, glutamate excitotoxicity, neuroinflammation, and effectively reversed injury‐induced gene pathways leading to chronic neurodegeneration. In addition to proving efficacious in well‐characterized animal TBI models, significantly mitigating cognitive and motor impairments, the drug also has demonstrated neuroprotective actions against ischemic stroke and the organophosphorus nerve agent and chemical weapon, soman. Conclusion In the light of its tolerability in AD clinical trials, PhenT is an agent that can be fast‐tracked for evaluation in not only civilian TBI, but also as a potentially protective agent in battlefield conditions where TBI and chemical weapon exposure are increasingly jointly occurring.
doi_str_mv 10.1111/cns.13274
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Albeit substantial impact has been made to improve our comprehension of the mechanisms that underpin the primary and secondary injury stages initiated by a TBI incident, this knowledge has yet to successfully translate into the development of an effective TBI pharmacological treatment. Developing consent suggests that a TBI can concomitantly trigger multiple TBI‐linked cascades that then progress in parallel and, if correct, the multifactorial nature of TBI would make the discovery of a single effective mechanism‐targeted drug unlikely. Discussion We review recent data indicating that the small molecular weight drug (−)‐phenserine tartrate (PhenT), originally developed for Alzheimer's disease (AD), effectively inhibits a broad range of mechanisms pertinent to mild (m) and moderate (mod)TBI, which in combination underpin the ensuing cognitive and motor impairments. In cellular and animal models at clinically translatable doses, PhenT mitigated mTBI‐ and modTBI‐induced programmed neuronal cell death (PNCD), oxidative stress, glutamate excitotoxicity, neuroinflammation, and effectively reversed injury‐induced gene pathways leading to chronic neurodegeneration. In addition to proving efficacious in well‐characterized animal TBI models, significantly mitigating cognitive and motor impairments, the drug also has demonstrated neuroprotective actions against ischemic stroke and the organophosphorus nerve agent and chemical weapon, soman. Conclusion In the light of its tolerability in AD clinical trials, PhenT is an agent that can be fast‐tracked for evaluation in not only civilian TBI, but also as a potentially protective agent in battlefield conditions where TBI and chemical weapon exposure are increasingly jointly occurring.</description><identifier>ISSN: 1755-5930</identifier><identifier>ISSN: 1755-5949</identifier><identifier>EISSN: 1755-5949</identifier><identifier>DOI: 10.1111/cns.13274</identifier><identifier>PMID: 31828969</identifier><language>eng</language><publisher>England: John Wiley &amp; Sons, Inc</publisher><subject>Alzheimer's disease ; Animal models ; Apoptosis ; Cell death ; Clinical trials ; Cognitive ability ; Drug therapy ; Excitotoxicity ; Geriatrics ; Head injuries ; Inflammation ; Ischemia ; Medicin och hälsovetenskap ; Molecular weight ; Morbidity ; Nerve agents ; Neurodegeneration ; Neurodegenerative diseases ; neuroinflammation ; Neuroprotection ; Original ; Oxidative stress ; Parkinson's disease ; phenserine ; preprogrammed neuronal cell death ; Soman ; Traumatic brain injury ; Young adults</subject><ispartof>CNS neuroscience &amp; therapeutics, 2020-06, Vol.26 (6), p.636-649</ispartof><rights>2019 The Authors. 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Albeit substantial impact has been made to improve our comprehension of the mechanisms that underpin the primary and secondary injury stages initiated by a TBI incident, this knowledge has yet to successfully translate into the development of an effective TBI pharmacological treatment. Developing consent suggests that a TBI can concomitantly trigger multiple TBI‐linked cascades that then progress in parallel and, if correct, the multifactorial nature of TBI would make the discovery of a single effective mechanism‐targeted drug unlikely. Discussion We review recent data indicating that the small molecular weight drug (−)‐phenserine tartrate (PhenT), originally developed for Alzheimer's disease (AD), effectively inhibits a broad range of mechanisms pertinent to mild (m) and moderate (mod)TBI, which in combination underpin the ensuing cognitive and motor impairments. 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Albeit substantial impact has been made to improve our comprehension of the mechanisms that underpin the primary and secondary injury stages initiated by a TBI incident, this knowledge has yet to successfully translate into the development of an effective TBI pharmacological treatment. Developing consent suggests that a TBI can concomitantly trigger multiple TBI‐linked cascades that then progress in parallel and, if correct, the multifactorial nature of TBI would make the discovery of a single effective mechanism‐targeted drug unlikely. Discussion We review recent data indicating that the small molecular weight drug (−)‐phenserine tartrate (PhenT), originally developed for Alzheimer's disease (AD), effectively inhibits a broad range of mechanisms pertinent to mild (m) and moderate (mod)TBI, which in combination underpin the ensuing cognitive and motor impairments. In cellular and animal models at clinically translatable doses, PhenT mitigated mTBI‐ and modTBI‐induced programmed neuronal cell death (PNCD), oxidative stress, glutamate excitotoxicity, neuroinflammation, and effectively reversed injury‐induced gene pathways leading to chronic neurodegeneration. In addition to proving efficacious in well‐characterized animal TBI models, significantly mitigating cognitive and motor impairments, the drug also has demonstrated neuroprotective actions against ischemic stroke and the organophosphorus nerve agent and chemical weapon, soman. Conclusion In the light of its tolerability in AD clinical trials, PhenT is an agent that can be fast‐tracked for evaluation in not only civilian TBI, but also as a potentially protective agent in battlefield conditions where TBI and chemical weapon exposure are increasingly jointly occurring.</abstract><cop>England</cop><pub>John Wiley &amp; Sons, Inc</pub><pmid>31828969</pmid><doi>10.1111/cns.13274</doi><tpages>14</tpages><orcidid>https://orcid.org/0000-0002-1122-9025</orcidid><orcidid>https://orcid.org/0000-0002-3032-1468</orcidid><oa>free_for_read</oa></addata></record>
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subjects Alzheimer's disease
Animal models
Apoptosis
Cell death
Clinical trials
Cognitive ability
Drug therapy
Excitotoxicity
Geriatrics
Head injuries
Inflammation
Ischemia
Medicin och hälsovetenskap
Molecular weight
Morbidity
Nerve agents
Neurodegeneration
Neurodegenerative diseases
neuroinflammation
Neuroprotection
Original
Oxidative stress
Parkinson's disease
phenserine
preprogrammed neuronal cell death
Soman
Traumatic brain injury
Young adults
title (−)‐Phenserine tartrate (PhenT) as a treatment for traumatic brain injury
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