Moreover, GSK-3β, as inactivated by Akt and overactive during AD, led to growth cone collapse and neurite retraction in vitro (Sayas et al., 1999) as well as postsynaptic protein (PSD-95) reductions, GluR1 loss and dendritic shortening in immature DG neurons plus microgliosis and inflammatory cytokine expression in the DG in vivo (Llorens-Martin et al., 2013). The gene discussed is GSK3B; the disease is Alzheimer disease.