Consistent with this, astrocyte malfunction results in impaired clearance of protein aggregates.89 In a more recent study, Kim et al demonstrated that impaired astrocytic autophagy leads to increased levels of Aβ aggregates and p-tau filaments, which correlate with poorer cognitive function in AD mouse models.90 Conversely, overexpression of autophagy-related genes in astrocytes is associated with a reduction in Aβ burden and improved behavioural symptoms in vivo,90 further highlighting the role of astrocytes in protein clearance. This evidence concerns the gene MAPT and Alzheimer disease.