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Sustained exposure to soluble amyloid β (Aβ42) oligomers is predicted to impair synaptic function in the hippocampal‐entorhinal circuit, signaling synaptic loss and precipitating cognitive impairment in Alzheimer's disease. Regional changes in overall patterns of protein phosphorylation are likely crucial to promote transition from a presymptomatic to a symptomatic state in response to accumulating...
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