RAB7A and Alzheimer disease: In this study, we first revealed that i) Cd exposure triggered autophagic flux blockade and exacerbated AD‐like pathology; ii) SIRT5 desuccinylated and activated RAB7A at the K31 residue to rescue the Cd‐provoked AD progression by maintaining the autophagic flux; and iii) the SIRT5 levels were mainly decreased in the neurons of AD patients, which confirmed the clinical relevance of SIRT5 in AD progression.