Mitochondrial Approaches for Neuroprotection
Identifieur interne : 000D47 ( Main/Exploration ); précédent : 000D46; suivant : 000D48Mitochondrial Approaches for Neuroprotection
Auteurs : Rajnish K. Chaturvedi [États-Unis] ; M. Flint Beal [États-Unis]Source :
- Annals of the New York Academy of SciencesMitochondria and Oxidative Stress in Neurodegenerative Disorders [ 0077-8923 ] ; 2008-12.
English descriptors
- KwdEn :
Abstract
A large body of evidence from postmortem brain tissue and genetic analysis in humans and biochemical and pathological studies in animal models (transgenic and toxin) of neurodegeneration suggest that mitochondrial dysfunction is a common pathological mechanism. Mitochondrial dysfunction from oxidative stress, mitochondrial DNA deletions, pathological mutations, altered mitochondrial morphology, and interaction of pathogenic proteins with mitochondria leads to neuronal demise. Therefore, therapeutic approaches targeting mitochondrial dysfunction and oxidative damage hold great promise in neurodegenerative diseases. This review discusses the potential therapeutic efficacy of creatine, coenzyme Q10, idebenone, synthetic triterpenoids, and mitochondrial targeted antioxidants (MitoQ) and peptides (SS‐31) in in vitro studies and in animal models of Parkinson's disease, Huntington's disease, amyotrophic lateral sclerosis, and Alzheimer's disease. We have also reviewed the current status of clinical trials of creatine, coenzyme Q10, idebenone, and MitoQ in neurodegenerative disorders. Further, we discuss newly identified therapeutic targets, including peroxisome proliferator‐activated receptor‐γ‐coactivator and sirtuins, which provide promise for future therapeutic developments in neurodegenerative disorders.
Url:
DOI: 10.1196/annals.1427.027
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Mitochondrial Approaches for Neuroprotection</title><author><name sortKey="Chaturvedi, Rajnish K" sort="Chaturvedi, Rajnish K" uniqKey="Chaturvedi R" first="Rajnish K." last="Chaturvedi">Rajnish K. Chaturvedi</name></author><author><name sortKey="Beal, M Flint" sort="Beal, M Flint" uniqKey="Beal M" first="M. Flint" last="Beal">M. Flint Beal</name></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:E8CE1CF1E5433502DE788DD5D77367C8C3B151F1</idno><date when="2008" year="2008">2008</date><idno type="doi">10.1196/annals.1427.027</idno><idno type="url">https://api.istex.fr/document/E8CE1CF1E5433502DE788DD5D77367C8C3B151F1/fulltext/pdf</idno><idno type="wicri:Area/Main/Corpus">000716</idno><idno type="wicri:Area/Main/Curation">000626</idno><idno type="wicri:Area/Main/Exploration">000D47</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Mitochondrial Approaches for Neuroprotection</title><author><name sortKey="Chaturvedi, Rajnish K" sort="Chaturvedi, Rajnish K" uniqKey="Chaturvedi R" first="Rajnish K." last="Chaturvedi">Rajnish K. Chaturvedi</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Neurology and Neuroscience, Weill Medical College of Cornell University, New York, New York</wicri:regionArea><placeName><region type="state">État de New York</region></placeName></affiliation></author><author><name sortKey="Beal, M Flint" sort="Beal, M Flint" uniqKey="Beal M" first="M. Flint" last="Beal">M. Flint Beal</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Neurology and Neuroscience, Weill Medical College of Cornell University, New York, New York</wicri:regionArea><placeName><region type="state">État de New York</region></placeName></affiliation></author></analytic><monogr></monogr><series><title level="j">Annals of the New York Academy of SciencesMitochondria and Oxidative Stress in Neurodegenerative Disorders</title><idno type="ISSN">0077-8923</idno><idno type="eISSN">1749-6632</idno><imprint><publisher>Blackwell Publishing Inc</publisher><pubPlace>Malden, USA</pubPlace><date type="published" when="2008-12">2008-12</date><biblScope unit="volume">1147</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="395">395</biblScope><biblScope unit="page" to="412">412</biblScope></imprint><idno type="ISSN">0077-8923</idno></series><idno type="istex">E8CE1CF1E5433502DE788DD5D77367C8C3B151F1</idno><idno type="DOI">10.1196/annals.1427.027</idno><idno type="ArticleID">NYAS1147027</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0077-8923</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Alzheimer's disease</term><term>Huntington's disease</term><term>PGC‐1α</term><term>Parkinson's disease</term><term>coenzyme Q10</term><term>creatine</term><term>triterpenoids</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">A large body of evidence from postmortem brain tissue and genetic analysis in humans and biochemical and pathological studies in animal models (transgenic and toxin) of neurodegeneration suggest that mitochondrial dysfunction is a common pathological mechanism. Mitochondrial dysfunction from oxidative stress, mitochondrial DNA deletions, pathological mutations, altered mitochondrial morphology, and interaction of pathogenic proteins with mitochondria leads to neuronal demise. Therefore, therapeutic approaches targeting mitochondrial dysfunction and oxidative damage hold great promise in neurodegenerative diseases. This review discusses the potential therapeutic efficacy of creatine, coenzyme Q10, idebenone, synthetic triterpenoids, and mitochondrial targeted antioxidants (MitoQ) and peptides (SS‐31) in in vitro studies and in animal models of Parkinson's disease, Huntington's disease, amyotrophic lateral sclerosis, and Alzheimer's disease. We have also reviewed the current status of clinical trials of creatine, coenzyme Q10, idebenone, and MitoQ in neurodegenerative disorders. Further, we discuss newly identified therapeutic targets, including peroxisome proliferator‐activated receptor‐γ‐coactivator and sirtuins, which provide promise for future therapeutic developments in neurodegenerative disorders.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>État de New York</li></region></list><tree><country name="États-Unis"><region name="État de New York"><name sortKey="Chaturvedi, Rajnish K" sort="Chaturvedi, Rajnish K" uniqKey="Chaturvedi R" first="Rajnish K." last="Chaturvedi">Rajnish K. Chaturvedi</name></region><name sortKey="Beal, M Flint" sort="Beal, M Flint" uniqKey="Beal M" first="M. Flint" last="Beal">M. Flint Beal</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Sante/explor/ParkinsonV1/Data/Main/Exploration
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000D47 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd -nk 000D47 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Wicri/Sante
|area= ParkinsonV1
|flux= Main
|étape= Exploration
|type= RBID
|clé= ISTEX:E8CE1CF1E5433502DE788DD5D77367C8C3B151F1
|texte= Mitochondrial Approaches for Neuroprotection
}}
| This area was generated with Dilib version V0.6.23. |  |