This preclinical mouse study found that age-associated sleep fragmentation and excessive sleepiness are ameliorated by dietary restriction, an effect that requires Prdm13 signaling in the dorsomedial hypothalamus.
Life Science Alliance · 17 authors, 12 centres
This summary was generated by AI from a single paper. It has not been reviewed by a clinician and is not clinical advice. Verify against the source before acting on it.
This preclinical mouse study found that age-associated sleep fragmentation and excessive sleepiness are ameliorated by dietary restriction, an effect that requires Prdm13 signaling in the dorsomedial hypothalamus.
The results show that old mice exhibit reduced wakefulness, increased NREM sleep, and significant sleep fragmentation compared to young mice. The study demonstrates that dietary restriction (DR) mitigates these age-associated sleep alterations, but this protective effect is absent in mice lacking Prdm13 signaling specifically in the dorsomedial hypothalamus (DMH). Furthermore, chemogenetic inhibition of Prdm13-expressing DMH neurons in young mice induced excessive sleepiness, mimicking a key age-related phenotype. A limitation is the direct translation to humans, as basic sleep architecture differs between nocturnal mice and diurnal humans. The findings suggest Prdm13 signaling in the DMH is a critical mediator of DR's benefits on age-related sleep dysfunction.