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In this setting, mitochondrial ROS from complex I/III sites, NOX2/NOX4 activity in microglia and cerebrovascular endothelium and impaired mitophagy (reduced removal of damaged mitochondria) converge to oxidize proteins and lipids, seed misfolding and aggregation (e.g., α-synuclein, Aβ) and blunt synaptic plasticity by altering redox-sensitive receptors, kinases and Ca²⁺ handling (Lee et al