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In general, our results showed that ethanol exposure may reduce the antioxidant capacity in the hippocampal of WT mice, leading to the occurrence of neuroinflammation, while in APP/PS1 mice, ethanol exposure further worsened this process by exacerbating the pathological progression of AD

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A commonly agreed upon the fact in the pathogenesis of SLE is the dysfunction of T cells, B cells, dendritic cells, macrophages, and neutrophils, likely triggered by genes and/or the environment [4]

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