Extracellular depositions of amyloid β (Aβ) peptides and accumulation of hyperphosphorylated tau in neurofibrillary tangles are believed to contribute to the pathophysiology of AD [2-4], while analogous misfolded proteins aggregate in other neurodegenerative diseases, including Huntington’s disease and amyotrophic lateral sclerosis (ALS) [5-7]. Here, MAPT is linked to amyotrophic lateral sclerosis.