Erik S. Musiek

Tumbly is an open-source, automated device for time-restricted feeding in mice, validated to maintain body weight and food intake with low error rates.

This study shows that C4 deficiency reduces amyloid plaques and neuroinflammation in a mouse AD model, suggesting C4's role in glial reactivity and pathology.

This study shows that astrocyte-specific deletion of Bmal1 disrupts circadian rhythms in perineuronal nets, synaptic plasticity, and learning behavior.

The paper introduces MACS-Calling Cards to map astrocyte-specific TF occupancy in vivo and finds BMAL1 binding is redistributed in a neurodegenerative disease model due to loss of cooperative TF interactions.

This study shows that disrupting the central circadian clock in 5xFAD mice under a light-dark cycle reduces amyloid plaque and tau phosphorylation, suggesting a complex interaction between circadian rhythms and Alzheimer's pathology.

The paper identifies cell-type and disease-specific circadian gene expression changes in glial cells under amyloid pathology or aging in mice.

The paper estimates circadian phases in human brain cells using single-nucleus RNA sequencing and finds disrupted ribosomal rhythms in Alzheimer's patients.

This study shows that Ms4a4a deficiency reduces amyloid beta pathology in mice by enhancing Aβ clearance, supported by increased MMP-9 production in microglia and human CSF data.

This study shows that inflammatory pain in mice alters sleep architecture and circadian rhythms, with effects dependent on the light cycle.

This study shows that microglia drive diurnal variation in BBB permeability during inflammation, with increased BBB breakdown following evening LPS injection.

This study shows that Kir6.2-KATP channels regulate glycolytic flux, neuronal activity, and sleep-wake transitions by modulating lactate dynamics and metabolic stability.

This study shows that the BMAL1-REV-ERB axis regulates complement expression and microglial synaptic phagocytosis in the hippocampus, with diurnal variation observed in wild-type mice.

This study shows BMAL1 regulates astrocyte activation and function through cell-autonomous and non-cell-autonomous mechanisms, impacting neuronal survival and brain health.