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Forschungsdatenbank PMU-SQQUID

Mutant alpha-synuclein exacerbates age-related decrease of neurogenesis.
Winner, B; Rockenstein, E; Lie, DC; Aigner, R; Mante, M; Bogdahn, U; Couillard-Despres, S; Masliah, E; Winkler, J;
Neurobiol Aging. 2008; 29(6): 913-925.
Originalarbeiten (Zeitschrift)


Couillard-Després Sébastien


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. (C) 2007 Elsevier Inc. All rights reserved.

Useful keywords (using NLM MeSH Indexing)



Cell Proliferation


Mice, Transgenic


Nerve Regeneration/physiology*


Olfactory Bulb/growth*


Parkinson Disease/physiopathology


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