Proteinaceous filaments of p-Tau are known to spread in a prion-like fashion in the human brain, leading to the detrimental formation of neurofibrillary tangles (NFTs) that contribute to AD pathology, correlate significantly with cognitive deficits in Alzheimer’s disease (AD), and contribute to distinguishing differences between AD and other tauopathies [28,29]. The gene discussed is MAPT; the disease is tauopathy.