| First Author | Winner B | Year | 2008 |
| Journal | Neurobiol Aging | Volume | 29 |
| Issue | 6 | Pages | 913-25 |
| PubMed ID | 17275140 | Mgi Jnum | J:140922 |
| Mgi Id | MGI:3814817 | Doi | 10.1016/j.neurobiolaging.2006.12.016 |
| Citation | Winner B, et al. (2008) Mutant alpha-synuclein exacerbates age-related decrease of neurogenesis. Neurobiol Aging 29(6):913-25 |
| abstractText | 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. |
