Social interaction rescues memory deficit in an animal model of Alzheimer’s disease by increasing BDNF-Dependent Hippocampal Neurogenesis

研究成果: Article同行評審

64 引文 斯高帕斯(Scopus)

摘要

It has been recognized that the risk of cognitive decline during aging can be reduced if one maintains strong social connections, yet the neural events underlying this beneficial effect have not been rigorously studied. Here, we show that amyloid precursor protein (APP) and presenilin 1 (PS1) double-transgenic (APP/PS1) mice demonstrate improvement in memory after they are cohoused with wild-type mice. The improvement was associated with increased protein and mRNA levels of BDNF in the hippocampus. Concomitantly, the number of BrdU+/NeuN+cells in the hippocampal dentate gyrus was significantly elevated after cohousing. Methylazoxymethanol acetate, a cell proliferation blocker, markedly reduced BrdU+and BrdU/NeuN+cells and abolished the effect of social interaction. Selective ablation of mitotic neurons using diphtheria toxin (DT) and a retrovirus vector encoding DT receptor abolished the beneficial effect of cohousing. Knockdown of BDNF by shRNA transfection blocked, whereas overexpression of BDNF mimicked the memory-improving effect. A tropomyosin-related kinase B agonist, 7,8-dihydroxyflavone, occluded the effect of social interaction. These results demonstrate that increased BDNF expression and neurogenesis in the hippocampus after cohousing underlie the reversal of memory deficit in APP/PS1 mice.

原文English
頁(從 - 到)16207-16219
頁數13
期刊Journal of Neuroscience
34
發行號49
DOIs
出版狀態Published - 2014 十二月 3

All Science Journal Classification (ASJC) codes

  • Neuroscience(all)

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