Genetic inactivation of Presenilins in neurons drives tau phosphorylation and aggregation in vivo by activating Akt/PKB and impairing proteasome-mediated tau degradation.
Our study reveals that impaired autophagy/proteasome-mediated tau elimination is a pathological feature of mutant PSEN1-linked familial AD, corticobasal degeneration and Pick’s disease dementias