[GSK-3beta: a central kinase for neurodegenerative diseases?].
Identifieur interne : 000A88 ( PubMed/Corpus ); précédent : 000A87; suivant : 000A89[GSK-3beta: a central kinase for neurodegenerative diseases?].
Auteurs : Agnès Petit-PaitelSource :
- Medecine sciences : M/S [ 0767-0974 ] ; 2010.
English descriptors
- KwdEn :
- Alzheimer Disease (enzymology), Alzheimer Disease (pathology), Amyloid beta-Protein Precursor (physiology), Apoptosis (physiology), Brain (enzymology), Brain (pathology), Carrier Proteins (physiology), Glycogen Synthase Kinase 3 (antagonists & inhibitors), Glycogen Synthase Kinase 3 (physiology), Glycogen Synthase Kinase 3 beta, Humans, Lewy Bodies, Mitochondria (physiology), Models, Neurological, Nerve Tissue Proteins (antagonists & inhibitors), Nerve Tissue Proteins (physiology), Neurodegenerative Diseases (drug therapy), Neurodegenerative Diseases (enzymology), Neurodegenerative Diseases (prevention & control), Neurofibrillary Tangles (enzymology), Parkinson Disease (enzymology), Phosphorylation, Plaque, Amyloid (enzymology), Presenilins (physiology), Protein Kinase Inhibitors (therapeutic use), Protein Processing, Post-Translational, alpha-Synuclein (physiology), tau Proteins (metabolism).
- MESH :
- chemical , antagonists & inhibitors : Glycogen Synthase Kinase 3, Nerve Tissue Proteins.
- chemical , metabolism : tau Proteins.
- chemical , physiology : Amyloid beta-Protein Precursor, Carrier Proteins, Glycogen Synthase Kinase 3, Nerve Tissue Proteins, Presenilins, alpha-Synuclein.
- drug therapy : Neurodegenerative Diseases.
- enzymology : Alzheimer Disease, Brain, Neurodegenerative Diseases, Neurofibrillary Tangles, Parkinson Disease, Plaque, Amyloid.
- pathology : Alzheimer Disease, Brain.
- physiology : Apoptosis, Mitochondria.
- prevention & control : Neurodegenerative Diseases.
- chemical , therapeutic use : Protein Kinase Inhibitors.
- chemical : Glycogen Synthase Kinase 3 beta, Humans, Lewy Bodies, Models, Neurological, Phosphorylation, Protein Processing, Post-Translational.
Abstract
Neurodegenerative diseases are more and more prevalent in our aging societies. There is strong evidence that glycogen synthase kinase (GSK)-3b plays a crucial role in Alzheimer's disease (AD). Indeed, it is involved in the regulation of the two major neuropathological hallmarks present in the brains of AD patients. Interestingly, the kinase has been implicated in multiple cellular processes and linked with the pathogenesis and neuronal loss in several neurodegenerative diseases, including Parkinson's and Huntington's diseases, in which abnormally elevated levels of GSK-3b activity have been reported. In this review, we will provide an overview of the current data pointing out the convergent role of GSK-3b in the neuropathological pathways of these diseases. We will also discuss the rationale for the development of specific inhibitors with therapeutic potentials for such devastating human diseases.
DOI: 10.1051/medsci/2010265516
PubMed: 20510151
Links to Exploration step
pubmed:20510151Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">[GSK-3beta: a central kinase for neurodegenerative diseases?].</title><author><name sortKey="Petit Paitel, Agnes" sort="Petit Paitel, Agnes" uniqKey="Petit Paitel A" first="Agnès" last="Petit-Paitel">Agnès Petit-Paitel</name><affiliation><nlm:affiliation>Institut de pharmacologie moléculaire et cellulaire, route des Lucioles, Sophia Antipolis, Valbonne, France. petit@ipmc.cnrs.fr</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2010">2010</date><idno type="RBID">pubmed:20510151</idno><idno type="pmid">20510151</idno><idno type="doi">10.1051/medsci/2010265516</idno><idno type="wicri:Area/PubMed/Corpus">000A88</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000A88</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">[GSK-3beta: a central kinase for neurodegenerative diseases?].</title><author><name sortKey="Petit Paitel, Agnes" sort="Petit Paitel, Agnes" uniqKey="Petit Paitel A" first="Agnès" last="Petit-Paitel">Agnès Petit-Paitel</name><affiliation><nlm:affiliation>Institut de pharmacologie moléculaire et cellulaire, route des Lucioles, Sophia Antipolis, Valbonne, France. petit@ipmc.cnrs.fr</nlm:affiliation></affiliation></author></analytic><series><title level="j">Medecine sciences : M/S</title><idno type="ISSN">0767-0974</idno><imprint><date when="2010" type="published">2010</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Alzheimer Disease (enzymology)</term><term>Alzheimer Disease (pathology)</term><term>Amyloid beta-Protein Precursor (physiology)</term><term>Apoptosis (physiology)</term><term>Brain (enzymology)</term><term>Brain (pathology)</term><term>Carrier Proteins (physiology)</term><term>Glycogen Synthase Kinase 3 (antagonists & inhibitors)</term><term>Glycogen Synthase Kinase 3 (physiology)</term><term>Glycogen Synthase Kinase 3 beta</term><term>Humans</term><term>Lewy Bodies</term><term>Mitochondria (physiology)</term><term>Models, Neurological</term><term>Nerve Tissue Proteins (antagonists & inhibitors)</term><term>Nerve Tissue Proteins (physiology)</term><term>Neurodegenerative Diseases (drug therapy)</term><term>Neurodegenerative Diseases (enzymology)</term><term>Neurodegenerative Diseases (prevention & control)</term><term>Neurofibrillary Tangles (enzymology)</term><term>Parkinson Disease (enzymology)</term><term>Phosphorylation</term><term>Plaque, Amyloid (enzymology)</term><term>Presenilins (physiology)</term><term>Protein Kinase Inhibitors (therapeutic use)</term><term>Protein Processing, Post-Translational</term><term>alpha-Synuclein (physiology)</term><term>tau Proteins (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Glycogen Synthase Kinase 3</term><term>Nerve Tissue Proteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>tau Proteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>Amyloid beta-Protein Precursor</term><term>Carrier Proteins</term><term>Glycogen Synthase Kinase 3</term><term>Nerve Tissue Proteins</term><term>Presenilins</term><term>alpha-Synuclein</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Neurodegenerative Diseases</term></keywords><keywords scheme="MESH" qualifier="enzymology" xml:lang="en"><term>Alzheimer Disease</term><term>Brain</term><term>Neurodegenerative Diseases</term><term>Neurofibrillary Tangles</term><term>Parkinson Disease</term><term>Plaque, Amyloid</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Alzheimer Disease</term><term>Brain</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Apoptosis</term><term>Mitochondria</term></keywords><keywords scheme="MESH" qualifier="prevention & control" xml:lang="en"><term>Neurodegenerative Diseases</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Protein Kinase Inhibitors</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>Glycogen Synthase Kinase 3 beta</term><term>Humans</term><term>Lewy Bodies</term><term>Models, Neurological</term><term>Phosphorylation</term><term>Protein Processing, Post-Translational</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Neurodegenerative diseases are more and more prevalent in our aging societies. There is strong evidence that glycogen synthase kinase (GSK)-3b plays a crucial role in Alzheimer's disease (AD). Indeed, it is involved in the regulation of the two major neuropathological hallmarks present in the brains of AD patients. Interestingly, the kinase has been implicated in multiple cellular processes and linked with the pathogenesis and neuronal loss in several neurodegenerative diseases, including Parkinson's and Huntington's diseases, in which abnormally elevated levels of GSK-3b activity have been reported. In this review, we will provide an overview of the current data pointing out the convergent role of GSK-3b in the neuropathological pathways of these diseases. We will also discuss the rationale for the development of specific inhibitors with therapeutic potentials for such devastating human diseases.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">20510151</PMID><DateCreated><Year>2010</Year><Month>05</Month><Day>31</Day></DateCreated><DateCompleted><Year>2010</Year><Month>08</Month><Day>11</Day></DateCompleted><DateRevised><Year>2016</Year><Month>11</Month><Day>25</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0767-0974</ISSN><JournalIssue CitedMedium="Print"><Volume>26</Volume><Issue>5</Issue><PubDate><Year>2010</Year><Month>May</Month></PubDate></JournalIssue><Title>Medecine sciences : M/S</Title><ISOAbbreviation>Med Sci (Paris)</ISOAbbreviation></Journal><ArticleTitle>[GSK-3beta: a central kinase for neurodegenerative diseases?].</ArticleTitle><Pagination><MedlinePgn>516-21</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1051/medsci/2010265516</ELocationID><Abstract><AbstractText>Neurodegenerative diseases are more and more prevalent in our aging societies. There is strong evidence that glycogen synthase kinase (GSK)-3b plays a crucial role in Alzheimer's disease (AD). Indeed, it is involved in the regulation of the two major neuropathological hallmarks present in the brains of AD patients. Interestingly, the kinase has been implicated in multiple cellular processes and linked with the pathogenesis and neuronal loss in several neurodegenerative diseases, including Parkinson's and Huntington's diseases, in which abnormally elevated levels of GSK-3b activity have been reported. In this review, we will provide an overview of the current data pointing out the convergent role of GSK-3b in the neuropathological pathways of these diseases. We will also discuss the rationale for the development of specific inhibitors with therapeutic potentials for such devastating human diseases.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Petit-Paitel</LastName><ForeName>Agnès</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Institut de pharmacologie moléculaire et cellulaire, route des Lucioles, Sophia Antipolis, Valbonne, France. petit@ipmc.cnrs.fr</Affiliation></AffiliationInfo></Author></AuthorList><Language>fre</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><VernacularTitle>GSK-3bêta :une kinase au coeur des maladies neuro-dégénératives?</VernacularTitle></Article><MedlineJournalInfo><Country>France</Country><MedlineTA>Med Sci 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