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To prevent excessive activation, complement is strongly controlled by C1-INH (CP), FH and FHL-1 (AP), and C4BP (CP and LP), vitronectin (Vn) clusterin, and FHR-1 (TP) (Fig

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In T2D-associated cognitive dysfunction, impaired mitophagy and impaired selective autophagy of other organelles (e.g., ER-phagy, pexophagy) contribute to synaptic damage and neuroinflammation