Article: Researchers from Harvard University, Center for Neurologic Diseases provide details of new studies and findings in the area of biochemistry.(Report)

Current study results from the report, 'Soluble oligomers of the amyloid beta-protein impair synaptic plasticity and behavior,' have been published. "During the last 25 years, neuropathological, biochemical, genetic, cell biological and even therapeutic studies in humans have all supported the hypothesis that the gradual cerebral accumulation of soluble and insoluble assemblies of the amyloid beta-protein (Abeta) in limbic and association cortices triggers a cascade of biochemical and cellular alterations that produce the clinical phenotype of Alzheimer's disease (AD). The reasons for elevated cortical Abeta42 levels in most patients with typical, late-onset AD are ...

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