Molecular mechanisms relevant to the neurite and synapse degeneration triggered by amyloid beta (Aβ) and occurring in AD include: increased phosphorylation, misfolding, cleavage and oligomerization of tau6,7; missorting of pathological forms of tau into dendrites and spines promoting deleterious protein–protein interactions8; and aberrant cofilin-mediated actin modification within spines9. The gene discussed is CFL1; the disease is Alzheimer disease.