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The hallmark pathological features of AD include the accumulation of β-amyloid (Aβ) peptides forming senile plaques and hyperphosphorylated tau aggregating into neurofibrillary tangles (NFTs), accompanied by synaptic dysfunction, neuronal loss, and chronic neuroinflammation (Agostinho et al., 2010
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Chronic copper peptide exposure without rest periods upregulates MMPs past the remodeling threshold
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