The aberrant accumulation of specific proteins, such as TDP-43 [16] and SOD1 [17] in ALS, amyloid β [18] and Tau [19] in AD, and α-synuclein [20] in PD, with similar proteinopathies seen in the chronic stage of ischemic stroke [21] can initiate a cascade of deleterious innate immunity processes that may contribute to the dysbiotic and dysfunctional GBA pathophysiological manifestations of NDDs. The gene discussed is MAPT; the disease is Alzheimer disease.