Decreased proliferation of hippocampal progenitor cells in APPswe/PS1dE9 transgenic mice

作者：Taniuchi Nobuhiko; Niidome Tetsuhiro^*; Goto Yasuaki; Akaike Akinori; Kihara Takeshi; Sugimoto Hachiro

来源：NeuroReport, 2007, 18(17): 1801-1805.

• Alzheimer's disease
• amyloid beta-peptide
• bromodeoxyuridine
• doublecortin
• gender difference
• hippocampus
• mice
• neurogenesis
• transgenic

A recent hypothesis suggests that there is impaired hippocampal neurogenesis in Alzheimer's disease. Here we examined the proliferation, the first stage in neurogenesis, of hippocampal progenitor cells in amyloid precursor protein with Swedish mutation and presenilin-I with deletion of exon 9 (APPswe/PS1dE9) transgenic mice. Compared with age-matched wild-type mice, transgenic mice at 5 months of age with low amyloid beta-peptide (A beta) levels and subtle A beta deposits showed normal proliferation of hippocampal progenitor cells; however, transgenic mice at 9 months of age with high A beta levels and numerous A beta deposits showed decreased proliferation of these cells. The number of proliferating cells in male transgenic mice was indistinguishable from that in female transgenic mice. These results indicate that neurogenesis is decreased with degrees of A beta pathology, and that there is no gender difference in their proliferation in APPswe/PS1dE9 transgenic mice.

• 出版日期2007-11-19