BMAL1 is an essential circadian regulator, and inactivation of brain and muscle arnt-like 1 (BMAL1) in PD model mice leads to marked motor dysfunction, loss of dopamine neurons in the dense substantia nigra, and reduction of dopamine transmitters, and allows for increased activation of microglia in the striatum In amyloid precursor protein knock-in model rats, the CLOCK/BMAL1 transcriptional negative feedback loop in microglia is impaired, and activation of the circadian clock gene Rev-erbα promotes inflammatory cytokine expression and cognitive deficits. This evidence concerns the gene BMAL1 and cognition.