In Alzheimer’s disease and tauopathies, aberrant activation of GSK-3β drives pathological tau hyperphosphorylation and neurofibrillary tangle formation [76], while phosphorylation by AKT at Ser9 acts upstream to inhibit GSK-3β, thereby promoting neuronal protection and synaptic stability. The gene discussed is GSK3B; the disease is early-onset autosomal dominant Alzheimer disease.