期刊
CELL REPORTS
卷 40, 期 13, 页码 -出版社
CELL PRESS
DOI: 10.1016/j.celrep.2022.111417
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资金
- NIH/NIA [AG20642, AG025135, P01 AG034906, AG058068]
- NIA T32 training grant [AG052374, PE-2016-02362694, PE-201602363073]
- Italian Ministry of Health
- NIH (NIA) [R01 AG056472, R01 AG057008, UH2/3 NS10012, R56 AG058655, 1R44 AG060826]
- College of Medicine at the University of Illinois, Chicago, and generous philanthropic contributions
The research suggests that fasting-mimicking diet cycles can help reduce cognitive decline and Alzheimer's disease pathology, with effects superior to protein restriction cycles. By reducing neuroinflammation and superoxide production, it delays cognitive decline in AD models.
The effects of fasting-mimicking diet (FMD) cycles in reducing many aging and disease risk factors indicate it could affect Alzheimer's disease (AD). Here, we show that FMD cycles reduce cognitive decline and AD pa-thology in E4FAD and 3xTg AD mouse models, with effects superior to those caused by protein restriction cycles. In 3xTg mice, long-term FMD cycles reduce hippocampal Ab load and hyperphosphorylated tau, enhance genesis of neural stem cells, decrease microglia number, and reduce expression of neuroinflamma-tory genes, including superoxide-generating NADPH oxidase (Nox2). 3xTg mice lacking Nox2 or mice treated with the NADPH oxidase inhibitor apocynin also display improved cognition and reduced microglia activation compared with controls. Clinical data indicate that FMD cycles are feasible and generally safe in a small group of AD patients. These results indicate that FMD cycles delay cognitive decline in AD models in part by reducing neuroinflammation and/or superoxide production in the brain.
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