Musiek et al. found that when Bmal1 was partially knockdown in primary neurons, these cells exhibited spontaneous neurodegeneration, revealing another cellular mechanism by which diminished Bmal1 expression contributed to neurodegenerative diseases (Musiek et al., 2013); further, Bmal1 deletion contributes to the impaired structure and dysfunction of synapses, as well as damaged cortical functional connectivity in brain regions that are seriously influenced in animal models of brain aging and AD (Musiek et al., 2013). The gene discussed is BMAL1; the disease is Alzheimer disease.