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HDAC3 and HDAC11, for instance, regulate oxidative stress responses and A metabolism, whereas HDAC7 contributes to tau pathology by suppressing lysosomal biogenesis through transcription factor EB (TFEB) deacetylation and by enhancing inflammatory signaling via the IKKNF-B pathway 31

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VPS35 gene mutations can lead to mitochondrial dysfunction and autophagy defects, preventing the timely clearance of aggregated proteins and thereby promoting Lewy body formation, followed by damage to dopaminergic (DA) neurons [18]