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Aβ is formed after sequential cleavage of the amyloid precursor protein (APP) by the β- and γ-secretases. APP is a transmembrane glycoprotein. Disregulation of APP metabolism — increasing either total Aβ levels or the relative concentration of the 42-amino acid form — seems to cause hereditary, early-onset Alzheimer's and is thought by many researchers to be involved in the etiology of the late-onset form.
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