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Amyloid β protein (Aβ) is one of the major components of senile plaques in the brain of Alzheimer disease patients and is derived from its precursor Amyloid precursor protein (APP), through the action of β- and γ-secretases (1). The APP is proteolytically processed to generate either the neurotoxic betaamyloid peptide (Aβ) or the secreted ectodomain APP alpha (sAPPα) (2). Secreted amyloid precursor protein-α (sAPPα) has several functions including the stimulation of neurite outgrowth, memory enhancement (3), however, its level is reduced during the pathogenesis of Alzheimer's disease,
1.Selkoe, D.J. Translating cell biology into therapeutic advances in Alzheimer's disease. Nature 399, A23–A31 (1999).
2. Tackenberg, C., Nitsch, R.M. The secreted APP ectodomain sAPPα, but not sAPPβ, protects neurons against Aβ oligomer-induced dendritic spine loss and increased tau phosphorylation. Mol Brain 12, 27 (2019).
3. Small DH, Nurcombe V, Reed G, Clarris H, Moir R, et al. (1994) A heparin-binding domain in the amyloid protein precursor of Alzheimer's disease is involved in the regulation of neurite outgrowth. J Neurosci 14: 2117–2127.