For example, while the identification of CTE neuropathologic change is based on the regional pattern and distribution of hyperphosphorylated tau (pTau), multiple other proteinopathies, among other types of brain lesions, are often observed coinciding with tau abnormalities in many of the cases characterized thus far [24], including β-amyloid pathologies [26], α-synuclein pathology [1] and TDP-43 proteinopathy [17]. This evidence concerns the gene MAPT and proteostasis deficiencies.