Importantly, in vivo models also outline possible mechanisms in which αSyn-GSK3β activity could contribute to a pathological feedback loop in AD; Aβ could increase GSK3β activity which in turn can induce tau phosphorylation and αSyn production (and heterotrimeric complexes), all of which (Aβ, tau, and αSyn) can seed the aggregation of one another, leading to potentially more Aβ production, GSK3β activation (via more Aβ and αSyn), tau phosphorylation, cellular dysfunction and apoptosis. This evidence concerns the gene GSK3B and Alzheimer disease.