Clinically, AD manifests as progressive decline in information processing domains, including memory, cognition, concentration, and executive function; pathologically, AD is characterized by parallel neurotoxic immuno-inflammation and cytotoxic protein oligomerization of Aβ/tau, culminating in interconnected, concomitant immunopathic (pro-inflammatory), and proteopathic (protein misfolding) pathogeneses. The gene discussed is MAPT; the disease is Alzheimer disease.