Age-dependent α-synuclein aggregation in the Microcebus murinus lemur primate.
Identifieur interne : 000879 ( PubMed/Curation ); précédent : 000878; suivant : 000880Age-dependent α-synuclein aggregation in the Microcebus murinus lemur primate.
Auteurs : Marie-Hélène Canron [France] ; Martine Perret ; Anne Vital ; Erwan Bézard ; Benjamin DehaySource :
- Scientific reports [ 2045-2322 ] ; 2012.
English descriptors
- KwdEn :
- Aging (metabolism), Aging (pathology), Alzheimer Disease (metabolism), Alzheimer Disease (pathology), Amyloid beta-Peptides (chemistry), Amyloid beta-Peptides (metabolism), Animals, Brain (metabolism), Brain (pathology), Brain Mapping, Cheirogaleidae, Disease Models, Animal, Female, Immunohistochemistry, Male, Parkinson Disease (metabolism), Parkinson Disease (pathology), Phosphorylation, Protein Folding, alpha-Synuclein (chemistry), alpha-Synuclein (metabolism).
- MESH :
- chemical , chemistry : Amyloid beta-Peptides, alpha-Synuclein.
- metabolism : Aging, Alzheimer Disease, Amyloid beta-Peptides, Brain, Parkinson Disease, alpha-Synuclein.
- pathology : Aging, Alzheimer Disease, Brain, Parkinson Disease.
- Animals, Brain Mapping, Cheirogaleidae, Disease Models, Animal, Female, Immunohistochemistry, Male, Phosphorylation, Protein Folding.
Abstract
Since age-dependent deposition of Aβ-amyloid has been reported in the Microcebusmurinus, we posited that this animal could as well be a model of age-related synucleinopathy. We characterized the distribution of Aβ-amyloid, α-synuclein and two of its modified forms in the brain of Microcebusmurinus aged from 1.5 to 10 years. Intracytoplasmic α-synuclein aggregates were observed only in aged animals in different brain regions, which were also phospho-Ser129 and nitrated α-synuclein immunoreactive. Age-dependent α-synuclein aggregation occurs spontaneously in mouse lemur primates. Microcebus murinus may provide a model to study age-associated α-synucleinopathy and for testing putative therapeutic interventions for both Alzheimer's and Parkinson's diseases.
DOI: 10.1038/srep00910
PubMed: 23205271
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We characterized the distribution of Aβ-amyloid, α-synuclein and two of its modified forms in the brain of Microcebusmurinus aged from 1.5 to 10 years. Intracytoplasmic α-synuclein aggregates were observed only in aged animals in different brain regions, which were also phospho-Ser129 and nitrated α-synuclein immunoreactive. Age-dependent α-synuclein aggregation occurs spontaneously in mouse lemur primates. Microcebus murinus may provide a model to study age-associated α-synucleinopathy and for testing putative therapeutic interventions for both Alzheimer's and Parkinson's diseases.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">23205271</PMID><DateCreated><Year>2012</Year><Month>12</Month><Day>03</Day></DateCreated><DateCompleted><Year>2013</Year><Month>05</Month><Day>06</Day></DateCompleted><DateRevised><Year>2015</Year><Month>02</Month><Day>19</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">2045-2322</ISSN><JournalIssue CitedMedium="Internet"><Volume>2</Volume><PubDate><Year>2012</Year></PubDate></JournalIssue><Title>Scientific reports</Title><ISOAbbreviation>Sci Rep</ISOAbbreviation></Journal><ArticleTitle>Age-dependent α-synuclein aggregation in the Microcebus murinus lemur primate.</ArticleTitle><Pagination><MedlinePgn>910</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1038/srep00910</ELocationID><Abstract><AbstractText>Since age-dependent deposition of Aβ-amyloid has been reported in the Microcebusmurinus, we posited that this animal could as well be a model of age-related synucleinopathy. We characterized the distribution of Aβ-amyloid, α-synuclein and two of its modified forms in the brain of Microcebusmurinus aged from 1.5 to 10 years. Intracytoplasmic α-synuclein aggregates were observed only in aged animals in different brain regions, which were also phospho-Ser129 and nitrated α-synuclein immunoreactive. Age-dependent α-synuclein aggregation occurs spontaneously in mouse lemur primates. 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Jan;28(1):61-70</RefSource><PMID Version="1">22753348</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neurobiol Aging. 1994 Mar-Apr;15(2):215-20</RefSource><PMID Version="1">7838294</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neurobiol Aging. 1998 Jan-Feb;19(1):65-9</RefSource><PMID Version="1">9562505</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Genes Brain Behav. 2006 Mar;5(2):120-30</RefSource><PMID Version="1">16507003</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Biol Chem. 2006 Oct 6;281(40):29739-52</RefSource><PMID Version="1">16847063</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Exp Gerontol. 2007 Mar;42(3):223-32</RefSource><PMID Version="1">17084573</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Acta Neuropathol. 2008 Apr;115(4):385-98</RefSource><PMID Version="1">18273623</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Curr Neurol Neurosci Rep. 2008 Jul;8(4):288-96</RefSource><PMID Version="1">18590612</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Ann Neurol. 2008 Dec;64 Suppl 2:S16-29</RefSource><PMID Version="1">19127585</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Prog Brain Res. 2010;183:115-45</RefSource><PMID Version="1">20696318</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Ageing Res Rev. 2012 Jan;11(1):150-62</RefSource><PMID Version="1">21802530</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Mov Disord. 2011 Jun;26(7):1198-1205</RefSource><PMID Version="1">22046592</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neurobiol Aging. 2011 May;32(5):894-906</RefSource><PMID Version="1">19564059</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>ILAR J. 2011;52(1):78-88</RefSource><PMID Version="1">21411860</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neurobiol Aging. 1992 Jan-Feb;13(1):99-105</RefSource><PMID Version="1">1542387</PMID></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName UI="D000375" MajorTopicYN="N">Aging</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000544" MajorTopicYN="N">Alzheimer Disease</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016229" MajorTopicYN="N">Amyloid beta-Peptides</DescriptorName><QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName><QualifierName UI="Q000378" 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