Examples include β-amyloid in alzheimer’s disease, misfolded huntington protein in Huntington’s disease, ubiquitinated protein aggregation in amyotrophic lateral sclerosis, tau and β-amyloid accumulation in multiple sclerosis plaques, α-synuclein accumulation in parkinson’s disease, and tau neurofibrillary tangles in traumatic brain injuries (Hussain et al., 2018). This evidence concerns the gene MAPT and Alzheimer disease.