期刊
AGING-US
卷 11, 期 19, 页码 8642-8663出版社
IMPACT JOURNALS LLC
DOI: 10.18632/aging.102352
关键词
Alzheimer's disease; APP/PS1 mice; trimethylamine-N-oxide; cognitive behavior; amyloid-beta
资金
- Natural Science Foundation of Heilongjiang Province of China [ZD2017017, H2016027]
- Harbin special fund for scientific and technological innovation talents [2016RAXYJ073]
Trimethylamine-N-oxide (TMAO), a metabolite of gut microbiota, has been implicated in the pathogenesis of Alzheimer's disease (AD). However, the mechanisms by which TMAO influence cognitive and pathological processes in the AD have not been investigated. In this study, we found that the circulating TMAO levels displayed an age-related increase in both WT and APP/PS1 mice and association with AD-like behavioral and pathological profile. Reduced TMAO by 3,3-Dimethyl-1-butanol (DMB) treatment ameliorated the cognitive deterioration and long-term potentiation (LTP) in APP/PS1 mice. Moreover, DMB treatment also induced a decrease in the Amyloid-beta (A beta)(1-42), beta-secretase, and beta-secretase-cleaved C-terminal fragment (beta CTF) levels in the hippocampus. Finally, the effects obtained after treatment with DMB were accompanied by a reduction in circulating clusterin levels and hippocampal neuroinflammatory status in APP/PS1 mice. These findings demonstrate that elevated circulating TMAO during the aging process might deteriorate cognitive function and pathology in APP/PS1 mice.
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