Studies in humans revealed particular pathways by which disease-specific protein pathology might spread through the CNS complementing experimental evidences (cell culture and animal models) of the molecular mechanisms of protein propagation in AD (involving tau and Aβ), FTLD-tau (involving tau), PD (involving α-synuclein), ALS and FTLD-TDP (both involving TDP-43) [46]. This evidence concerns the gene MAPT and amyotrophic lateral sclerosis.