Therefore, we proposed that patterns of HP-tau, amyloid-β and α-synuclein in clinicopathologically diagnosed dementia groups could be investigated to identify key hubs of these specific brain pathologies, which can then be related to the clinical phenotype, particularly cognition, given the likely centrality of HP-tau and amyloid-β in driving cognitive dysfunction in AD and LB dementia.11,19-21. This evidence concerns the gene MAPT and Alzheimer disease.