There is a vast literature on the role of beta amyloid (Aβ) peptides in the pathogenesis of Alzheimer's disease. However, there is a paucity of research on the potential physiological functions of these evolutionarily conserved products of the Aβ precursor protein. Based on previous studies in neuroblastoma cells, we hypothesized that Aβ may contribute to the proliferation of somatic cells.
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