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The human genome contains only about double the number of genes in comparison to the fruit fly. This necessitates efficient recurrent usage of the same molecular components to participate in different processes. When the same proteins are used for different signaling pathways, it may be conceivable that if they go awry the phenotypic consequences may vary to a great extent. The involvement of amyloid β precursor protein, Presenilin-1, and Tau in the pathogenesis of Alzheimer's disease is well established. Here we are highlighting a second facet of their function, their participation in developmental and adult neuronal migration. We propose that the prevalent and early Anosmia found in Alzheimer's patients may be due in part to malfunctioning of the above-mentioned proteins.