Are cortical Lewy bodies and Aβ burden associated with prevalence and timing of dementia in Lewy body diseases?
High CLB burden is a key neuropathological substrate of dementia in LBD. Elevated cortical LB pathology and Aβ plaque deposition are both correlated with a faster progression to dementia. The higher CLB load in the temporal and parietal regions, which seems to be a distinguishing feature of DLB, may account for the shorter latency to dementia and could be mediated by the APOE ϵ4 allele.
E2V and DG treatment may inhibit arterial inflammation by regulating ERβ-related signaling pathways.