Furthermore, binding of the tracers to multiple β-sheet structures could limit the interpretation of studies investigating the association between those different co-existent pathologies (i.e., amyloid-β, tau, α-synuclein, and TDP-43) in patients with cognitive complaints, and especially those looking into the association between tau and amyloid-β in AD (studies discussed below), where both pathologies are involved and are often colocalized. This evidence concerns the gene MAPT and Alzheimer disease.