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Winner, B.* ; Rockenstein, E.* ; Lie, D.C. ; Aigner, R.* ; Mante, M.* ; Bogdahn, U.* ; Couillard-Despres, S.* ; Masliah, E.* ; Winkler, J.*

Mutant alpha-synuclein exacerbates age-related decrease of neurogenesis.

Neurobiol. Aging 29, 913-925 (2008)
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Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
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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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Cell death; Neural stem/progenitor cells; Neurogenesis; Olfactory bulb; Parkinson's disease; Synucleinopathy
ISSN (print) / ISBN 0197-4580
e-ISSN 1558-1497
Zeitschrift Neurobiology of Aging
Quellenangaben Band: 29, Heft: 6, Seiten: 913-925 Artikelnummer: , Supplement: ,
Verlag Elsevier
Verlagsort New York, NY [u.a.]
Begutachtungsstatus Peer reviewed