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Open Access Green as soon as Postprint is submitted to ZB.
Mutant alpha-synuclein exacerbates age-related decrease of neurogenesis.
Neurobiol. Aging 29, 913-925 (2008)
In Parkinson disease, wild-type alpha-synuclein accumulates during aging, whereas alpha-synuclein mutations lead to an early onset and accelerated course of the disease. The generation of new neurons is decreased in regions of neurogenesis in adult mice overexpressing wild-type human alpha-synuclein. We examined the subventricular zone/olfactory bulb neurogenesis in aged mice expressing either wild-type human or A53T mutant alpha-synuclein. Aging wild-type and mutant alpha-synuclein-expressing animals generated significantly fewer new neurons than their non-transgenic littermates. This decreased neurogenesis was caused by a reduction in cell proliferation within the subventricular zone of mutant alpha-synuclein mice. In contrast, no difference was detected in mice overexpressing the wild-type allele. Also, more TUNEL-positive profiles were detected in the subventricular zone, following mutant alpha-synuclein expression and in the olfactory bulb, following wild-type and mutant alpha-synuclein expression. The impaired neurogenesis in the olfactory bulb of different transgenic alpha-synuclein mice during aging highlights the need to further explore the interplay between olfactory dysfunction and neurogenesis in Parkinson disease.
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Publication type
Article: Journal article
Document type
Scientific Article
Keywords
Cell death; Neural stem/progenitor cells; Neurogenesis; Olfactory bulb; Parkinson's disease; Synucleinopathy
Language
english
Publication Year
2008
HGF-reported in Year
2008
ISSN (print) / ISBN
0197-4580
e-ISSN
1558-1497
Journal
Neurobiology of Aging
Quellenangaben
Volume: 29,
Issue: 6,
Pages: 913-925
Publisher
Elsevier
Publishing Place
New York, NY [u.a.]
Reviewing status
Peer reviewed
Institute(s)
Institute of Developmental Genetics (IDG)
PSP Element(s)
G-551100-001
Scopus ID
42649103331
Erfassungsdatum
2008-10-24