Furthermore, there is a knowledge gap concerning whether genetic associations, such as the H1/H2 haplotype of the microtubule associated tau (MAPT) gene20,21or the transmembrane protein 106B (TMEM106B), and biochemical features of aggregated tau associated with PSP and CBD pathology22 are associated with 4R tauopathies underlying PAOS, or whether genetic mutations or polymorphisms in TMEM106B associated with degenerative diseases such as PSP, CBD, Picks disease (PiD) and  the protein TDP-43, play any role in PAOS. This evidence concerns the gene MAPT and frontotemporal dementia.