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Despite a decade long universal publication in favor of the view on amyloid-beta (A beta) as Alzheimer's disease culprit (solely neurotoxic for neurons and brain tissue), current scientific evidence leaves little doubt that A beta serves an essential role at synapse and in synaptic structure-functional plasticity that underlie learning and memory. Therefore, the change of A beta biology in Alzheimer's disease (as well as in a number of other human pathologies, including cardiovascular disease,pmid:15190681 fatcat:3p7e5blhung4bdsy5ghbykjnxq