摘要 : Background: Alzheimer's disease (AD) is a neurodegenerative illness, with several peripheral pathological signs such as accumulation of amyloid-beta (A beta) plaques in the kidney. Alterations of transforming growth factor beta (T... 展开 Background: Alzheimer's disease (AD) is a neurodegenerative illness, with several peripheral pathological signs such as accumulation of amyloid-beta (A beta) plaques in the kidney. Alterations of transforming growth factor beta (TGF beta) signaling in the kidney can induce fibrosis, thus disturbing the elimination of A beta. Objective: A protective role of increased physical activity has been proven in AD and in kidney fibrosis, but it is not clear whether TGF beta signalization is involved in this effect. Methods: The effects of long-term training on fibrosis were investigated in the kidneys of mice representing a model of AD (B6C3-Tg(APPswe,PSEN1dE9)85Dbo/J) by comparing wild type and AD organs. Alterations of canonical and non-canonical TGF beta signaling pathways were followed with PCR, western blot, and immunohistochemistry. Results: Accumulation of collagen type I and interstitial fibrosis were reduced in kidneys of AD mice after long-term training. AD induced the activation of canonical and non-canonical TGF beta pathways in non-trained mice, while expression levels of signal molecules of both TGF beta pathways became normalized in trained AD mice. Decreased amounts of phosphoproteins with molecular weight corresponding to that of tau and the cleaved C-terminal of A beta PP were detected upon exercising, along with a significant increase of PP2A catalytic subunit expression. Conclusion: Our data suggest that physical training has beneficial effects on fibrosis formation in kidneys of AD mice and TGF beta signaling plays a role in this phenomenon. 收起