Abstract：
: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.
journal_name
Neurobiol Agingjournal_title
Neurobiology of agingauthors
Winner B,Rockenstein E,Lie DC,Aigner R,Mante M,Bogdahn U,Couillard-Despres S,Masliah E,Winkler Jdoi
10.1016/j.neurobiolaging.2006.12.016subject
Has Abstractpub_date
2008-06-01 00:00:00pages
913-25issue
6eissn
0197-4580issn
1558-1497pii
S0197-4580(07)00004-8journal_volume
29pub_type
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