Preparing your results

Our searching services are busy right now. Your search will reload in five seconds.

X
Forgot Password

If you have forgotten your password you can enter your email here and get a temporary password sent to your email.

Overexpression of wild type but not an FAD mutant presenilin-1 promotes neurogenesis in the hippocampus of adult mice.

Neurobiology of disease | Jun 24, 2002

http://www.ncbi.nlm.nih.gov/pubmed/12079399

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.

Pubmed ID: 12079399 RIS Download

Mesh terms: Aging | Alzheimer Disease | Animals | Cell Count | Cell Differentiation | Cell Survival | Hippocampus | Humans | Membrane Proteins | Mice | Mice, Inbred C57BL | Mice, Inbred DBA | Mice, Transgenic | Mutation | Neurons | Presenilin-1 | Stem Cells

Research resources used in this publication

None found

Research tools detected in this publication

None found

Data used in this publication

None found

Associated grants

  • Agency: NIA NIH HHS, Id: AG05138
  • Agency: NIA NIH HHS, Id: AG08200
  • Agency: NIA NIH HHS, Id: AG14392
  • Agency: NIA NIH HHS, Id: AG17926

Mouse Genome Informatics (Data, Gene Annotation)

Publication data is provided by the National Library of Medicine ® and PubMed ®. Data is retrieved from PubMed ® on a weekly schedule. For terms and conditions see the National Library of Medicine Terms and Conditions.