- 作者：Susanne A. Wolf ; Golo Kronenberg ; Kathrin Lehmann ; Aaron Blankenship ; Rupert Overall ; Matthias Staufenbiel ; Gerd Kempermann
- 刊名：Biological Psychiatry
- 出版年：2006
- 期刊代码：34_00063223
- 类别：med
- 出版时间：15 December 2006
- 卷：60
- 期：12
- 页码：1314-1323
- 文件大小：1694 K
Background
In aging mice, activity maintains hippocampal plasticity and adult hippocampal neurogenesis at a level corresponding to a younger age. Here we studied whether physical exercise and environmental enrichment would also affect brain plasticity in a mouse model of Alzheimer’s disease (AD).Methods
Amyloid precursor protein (APP)-23 mice were housed under standard or enriched conditions or in cages equipped with a running wheel. We assessed β-amyloid plaque load, adult hippocampal neurogenesis, spatial learning, and mRNA levels of trophic factors in the brain.
Results
Despite stable β-amyloid plaque load, enriched-living mice showed improved water maze performance, an up-regulation of hippocampal neurotrophin (NT-3) and brain-derived neurotrophic factor (BDNF) and increased hippocampal neurogenesis. In contrast, despite increased bodily fitness, wheel-running APP23 mice showed no change in spatial learning and no change in adult hippocampal neurogenesis but a down-regulation of hippocampal and cortical growth factors.
Conclusions
We conclude that structural and molecular prerequisites for activity-dependent plasticity are preserved in mutant mice with an AD-like pathology. Our study might help explain benefits of activity for the aging brain but also demonstrates differences between physical and more cognitive activity. It also suggests a possible cellular correlate for the dissociation between structural and functional pathology often found in AD.