| First Author | Wen PH | Year | 2002 |
| Journal | Neurobiol Dis | Volume | 10 |
| Issue | 1 | Pages | 8-19 |
| PubMed ID | 12079399 | Mgi Jnum | J:100959 |
| Mgi Id | MGI:3590101 | Doi | 10.1006/nbdi.2002.0490 |
| Citation | Wen PH, et al. (2002) Overexpression of wild type but not an FAD mutant presenilin-1 promotes neurogenesis in the hippocampus of adult mice. Neurobiol Dis 10(1):8-19 |
| abstractText | Mutations in the presenilin-1 (PS-1) gene are one cause of familial Alzheimer's disease (FAD). However, the functions of the PS-1 protein as well as how PS-1 mutations cause FAD are incompletely understood. Here we investigated if neuronal overexpression of wild-type or FAD mutant PS-1 in transgenic mice affects neurogenesis in the hippocampus of adult animals. We show that either a wild-type or an FAD mutant PS-1 transgene reduces the number of neural progenitors in the dentate gyrus. However, the wild-type, but not the FAD mutant PS-1 promoted the survival and differentiation of progenitors leading to more immature granule cell neurons being generated in PS-1 wild type expressing animals. These studies suggest that PS-1 plays a role in regulating neurogenesis in adult hippocampus and that FAD mutants may have deleterious properties independent of their effects on amyloid deposition. |
