Because the repeat domain of Tau forms the core of paired helical filaments in Alzheimer disease and also assembles more readily than full-length Tau into bona fide paired helical filaments in vitro[13], [14], we employed recombinant human Tau fragment Tau244–372 consisting of the four-repeat microtubule binding domain for studying kinetics of Tau fibril formation. This evidence concerns the gene MAPT and early-onset autosomal dominant Alzheimer disease.