involves vascular inflammation. in the brain in the case of alzheimers. <theorized.> more readily applicable to vascular dementia.

and then, in the rest of the cardiovascular system in artherosclerosis/CVD. (reducing inflammation = reducing plaques laid down over them , that are being attracted to inflamed areas.. or piling up dead macrophages and foamy cells that went there to help.)

im not aware that either of these are totally settled at this time other than some anecdotal data on slowing down MACE and progression in the latter case (CVD). some cardiologists are believers and incorporating it in treatment now. its not an industry best practice but for those who are prescribing it for this reason, theyre citing a 20-40% reduction in events over 2-5 years.

or put another way. we know inflammation plays a role in CVD and we have a pretty reliable biomarker (CRP ) for whether this holds water and the inflammation is reduced by glp-1 agonists. not to be controversial or speak to medical matters but its my understanding that it does.

its role in dementia/alzheimers is just one of the ideas out there but the reasoning and the conclusions are kind of in the same neighborhood.