Data from: Scheduled feeding improves behavioral outcomes and reduces inflammation in a mouse model of fragile X syndrome

Fragile X syndrome (FXS), a leading inherited cause of intellectual
disability and autism, is frequently accompanied by sleep and circadian
rhythm disturbances. In this study, we comprehensively characterized these
disruptions and evaluated the therapeutic potential of a circadian-based
intervention in the fragile X mental retardation 1 (FMR1) knockout (KO)
mouse. The Fmr1 KO mice exhibited fragmented sleep, impaired locomotor
rhythmicity, and attenuated behavioral responses to light, linked to an
abnormal retinal innervation and reduction of light-evoked neuronal
activation in the suprachiasmatic nucleus. Behavioral testing revealed
significant deficits in social memory and increased repetitive behaviors
in the mutants, which correlated with sleep fragmentation. Remarkably, a
scheduled feeding paradigm (6-hour feeding/18-hour fasting) significantly
enhanced circadian rhythmicity, consolidated sleep, and improved social
deficits and repetitive behaviors in the Fmr1 KO mice. This intervention
also normalized the elevated levels of some pro-inflammatory cytokines,
including IL-12 and IFN-γ, in the mutants’ blood, suggesting that its
benefits extend to inflammatory pathways. These findings highlight the
interplay between circadian disruption, behavior, and an inflammatory
response in FXS, and provide compelling evidence that time-restricted
feeding may serve as a promising non-pharmacological approach for
improving core symptoms in neurodevelopmental disorders.