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By binding to PPAR, caudatin increased both lysosomal biogenesis and autophagic flux, resulting in enhanced clearance of A aggregates and hyperphosphorylated Tau aggregates in neuronal and microglial cell types (Figure 3B)

This translocation provides luminal microbes, and their associated products, with an opportunity to migrate to distant organs and cause IRs that encourage the development of AD or exacerbate disease pathologies

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