Imposing specific feeding windows has demonstrated a protective effect on the cerebral health of mice, mitigating some of the neurological damage characteristic of Alzheimer’s disease and bolstering their memory retention. Findings from this study backed by the National Institute on Aging (NIA) and featured in the journal Cell Metabolism, indicate that such fasting protocols could serve as a defense against Alzheimer’s by reprogramming the circadian clock—our intrinsic timekeeper regulating daily physiological and behavioral patterns—and altering gene expression in the brain. Disruptions in these circadian rhythms are prevalent among Alzheimer’s patients, often resulting in a progressive cognitive downturn, nightly disorientation, and sleep disturbances. Emerging studies endorse time-restricted feeding (TRF), a variant of intermittent fasting, as a potential means to realign these rhythms, thus enhancing sleep quality, metabolic processes, and overall health.
In the current research, a team of scientists from the University of California, San Diego examined the impact of TRF on mice genetically modified to express elevated levels of beta-amyloid – the hallmark protein aggregating in the brains of those with Alzheimer’s. These mice exhibited numerous Alzheimer’s-like symptoms, notably the accumulation of substantial beta-amyloid deposits in critical areas of the brain.
The team of researchers explored the impact of time-restricted feeding (TRF) by subjecting both Alzheimer’s model mice and unaffected control mice to either a regimented feeding schedule — allocating a six-hour window for feeding followed by an eighteen-hour fast — or a diet without time constraints.
Preliminary findings revealed that the Alzheimer’s mice experienced a disturbance in their circadian rhythms, and TRF seemed to mitigate some of these disruptions. Notably, Alzheimer’s mice on the TRF regimen exhibited reduced levels of activity during rest periods compared to their counterparts with no feeding restrictions, a pattern more closely resembling the control mice with unrestricted diets.
Further inquiry indicated that TRF played a role in diminishing several pathological indicators associated with Alzheimer’s. Not only did the restricted diet group display fewer beta-amyloid plaques, which are indicative of cerebral degeneration in Alzheimer’s, but they also showed decreased levels of brain inflammation. These positive effects of TRF were consistently observed, even in another strain of Alzheimer’s mice that typically exhibited disease markers earlier than those in the initial study group.
In parallel research involving an alternate subset of Alzheimer’s model mice, time-restricted feeding (TRF) also appeared to bolster cognitive functions. These mice, when subjected to a TRF regimen, showcased enhanced memory, particularly in recognizing the placement of objects within a maze—a performance that mirrored that of the control group and surpassed that of their unrestricted-diet counterparts. Crucially, all mice consumed identical amounts of food, ruling out caloric intake as a factor in these cognitive improvements.
Subsequent genetic examinations of the first Alzheimer’s mouse model revealed that TRF could potentially reverse numerous Alzheimer’s-related genetic alterations. The gene expression profile in the brains of Alzheimer’s mice on TRF significantly resembled that observed in control mice, distinctly contrasting with Alzheimer’s mice given unlimited food access.
Collectively, this research indicates that TRF may recalibrate disrupted circadian rhythms and decelerate the various behavioral, cognitive, and genetic disturbances linked to Alzheimer’s in murine models. While further studies are necessitated to assess TRF’s effects on human Alzheimer’s patients, these preliminary mouse-model results highlight TRF’s potential as a non-pharmaceutical approach to mitigate or perhaps even arrest the progression of Alzheimer’s disease.