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Amyloid precursor protein (APP), a key molecule of Alzheimer disease, is metabolized in 2 antagonist pathways generating the soluble APP alpha (sAPPα) having neuroprotective properties and the beta amyloid (Aβ) peptide at the origin of neurotoxic oligomers, particularly Aβ1–42. Whether extracellular Aβ1–42 oligomers modulate the formation and secretion of sAPPα is not known. We report here that the...
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