Circadian modulation by time-restricted feeding rescues brain pathology and improves memory in mouse models of Alzheimer’s disease

Aug 22, 2023Cell metabolism

Limiting eating times to daily cycles helps improve brain damage and memory in Alzheimer’s mouse models

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Abstract

Time-restricted feeding (TRF) improved key components of Alzheimer's disease pathology in two transgenic mouse models.

TRF reduced amyloid deposition and increased the clearance of amyloid-beta (Aβ42).
Improvements in sleep and memory were observed alongside TRF.
TRF normalized daily patterns of gene expression linked to Alzheimer's disease and neuroinflammation.
The findings suggest that TRF may have effects beyond metabolism, potentially ameliorating neurodegeneration.
This intervention could modify the trajectory of Alzheimer's disease progression.

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Circadian disruptions impact nearly all people with Alzheimer's disease (AD), emphasizing both their potential role in pathology and the critical need to investigate the therapeutic potential of circadian-modulating interventions. Here, we show that time-restricted feeding (TRF) without caloric restriction improved key disease components including behavioral timing, disease pathology, hippocampal transcription, and memory in two transgenic (TG) mouse models of AD. We found that TRF had the remarkable capability of simultaneously reducing amyloid deposition, increasing Aβ42 clearance, improving sleep and memory, and normalizing daily transcription patterns of multiple genes, including those associated with AD and neuroinflammation. Thus, our study unveils for the first time the pleiotropic nature of timed feeding on AD, which has far-reaching effects beyond metabolism, ameliorating neurodegeneration and the misalignment of circadian rhythmicity. Since TRF can substantially modify disease trajectory, this intervention has immediate translational potential, addressing the urgent demand for accessible approaches to reduce or halt AD progression.

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Circadian modulation by time-restricted feeding rescues brain pathology and improves memory in mouse models of Alzheimer’s disease

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