Thus, the loss of astrocytic Bmal1 is not sufficient to trigger astrocyte-dependent plaque removal processes in AD, whereas in PD models, BMAL1 loss in astrocytes reduces accumulation of pathological proteins, highlighting a differential role for BMAL1 in the pathogenesis of these two neurodegenerative diseases [90,91]. This evidence concerns the gene BMAL1 and neurodegenerative disease.