Alternate-day fasting reduced Parkinson-like α-synuclein pathology and inflammation in a mouse model, with gut microbiota implicated in the effect.
Evidence
This MPTP-induced subacute mouse study found optimal neuroprotection after 16 weeks of ADF and similar protection after fecal microbiota transplantation from ADF mice.
Caveat
The findings come from a mouse model with microbiota-transfer experiments, so they do not establish clinical benefit in human Parkinson's disease.
Simplified
Dietary restrictions like alternate-day fasting (ADF) can counteract several age-related disorders, but its role in Parkinson's disease (PD) is still controversial. Recent findings highlight the imbalances in the in PD, herein, we aim to study whether ADF can confer protection in PD mice through the gut-brain axis. Firstly, we assessed the neuroprotective effect of ADF in a time-dependent manner and found that 16 -week ADF could confer the optimal neuroprotection by preserving dopaminergic neurons and reducing the level of α‑synuclein (α‑syn) in the substantia nigra (SN), and it could decrease inflammatory cytokine levels in both the brain and the gut. Furthermore, ADF reshaped gut microbial composition and altered metabolites associated with PD. Relative abundances of several intestinal flora, including Alistipes, Helicobacter and Lactobacillus, were identified as potential mediators. In addition, we conducted fecal microbiota transplantation (FMT) to further investigate the role of the gut-brain axis in the neuroprotective effects of ADF. Notably, we found that FMT from ADF mice conferred equal protection to ADF in ameliorating the pathology and inflammation in both the brain and the gut. Collectively, our findings suggest that the microbiota-gut-brain axis is crucial to the neuroprotective effect of ADF in PD.
Key numbers
16 weeks
Decrease in α-synuclein Levels
Optimal duration of to achieve neuroprotective effects in PD mice.
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Fecal Microbiota Transplantation Effectiveness
FMT from mice alleviates neurotoxicity in PD models.
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