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In Alzheimers disease, the production of pro-inflammatory factors and A can over-activate microglia, secrete inflammatory factors and neurotoxins, and then induce neuronal damage and even apoptosis, thereby triggering Alzheimers disease

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LOXL2-overexpressing A7r5 cells showed significant overlap of BHZ incorporation and endogenous collagen I and IV deposited in the ECM (Fig