The term “Tauopathy” has been used as a descriptor for any neurologic syndrome that feature abnormal forms of this protein; for example, Alzheimer’s disease (AD) can be considered a secondary Tauopathy where neurofibrillary tangles (NFTs) containing hyperphosphorylated forms of Tau are a hallmark feature, yet where MAPT is free of mutations that alter protein structure or spliced forms. This evidence concerns the gene MAPT and early-onset autosomal dominant Alzheimer disease.