The recent detection of potential hybrid oligomers composed of Aβ and otherneurodegenerative disease associated proteins such as α-synuclein, TDP-43 and PrPfrom human AD post mortem brains suggest that Aβ oligomers may act as a template forthe aggregation of other proteins generating a secondary amyloidosis 14, 15, 62. This evidence concerns the gene TARDBP and glycogen storage disease VI.