ABL1 and Alzheimer disease: Since chemical and genetic inhibition of c-Abl activity showed a reduction in PSD-95 tyrosine 533 phosphorylation and an increase in PSD-95 clustering and synapse formation [45], it has been suggested that excessive activity of Rho family small GTPase Rac1 negatively affects synaptic and cognitive function and leads to mental retardation in AD [60].