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[After much initial debate for and against the role of amyloid in Alzheimer's disease (AD), mutations on the amyloid precursor protein (APP) and processing pathways that increase levels of the amyloid b peptide of 42 residues (Abeta42) have established that faulty function or processing of these proteins are responsible for AD pathogenesis.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine.
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