Furthermore, post-mortem brain tissue analysis has shown a significant upregulation of the UPR mediator GRP78/BiP in the cingulate gyrus and parietal cortex of DLB and PDD patients [141], underscoring the relevance of UPR activation in the etiology of LBD and its potential implications for disease pathology. This evidence concerns the gene HSPA5 and Lewy body dementia.