Conversely, in patients with cognitive impairment not due to AD, no immune and endothelial MGBA mediators were associated with amyloid and tau pathology and neurodegeneration and many of them were associated with cognitive performance (sPECAM-1, sP-Selectin, IL1β, and decreased of IL10), suggesting that the link between GM alterations and cognitive impairment in non-AD patients likely involved different pathways than AD. This evidence concerns the gene IL1B and Cognitive impairment.