Global postnatal BMAL1-KO in mouse models of tauopathy or alpha-synucleinopathy suppresses the aggregation of both tau protein and αSyn, reduces microgliosis and related pathology, while astrocytic BMAL1-KO in vivo prevents αSyn and tau accumulation by increasing astrocyte activation and the expression of the Bag3 gene (an activator of macroautophagy) and, as a result, the phagocytosis of pathological proteins [90]. Here, BMAL1 is linked to synucleinopathy.