The typical pathology of TBI-associated AD is similar to that of other causes, i.e., amyloid β-peptide (Aβ) aggregates into extracellular amyloid plaques and hyperphosphorylated tau accumulates intracellularly to form neurofibrillary tangles [97], and Lewy bodies (LBs) and Lewy neurites (LNs) in PD contain oligomerized α-synuclein (α-syn) [98]. The gene discussed is MAPT; the disease is Alzheimer disease.