A phenotype of microglial activation characterized by elevation of CD86, IL‐10, TNFα, IL‐1β, IL‐6, and decrease in IL‐12, already in asymptomatic patients below age 40, has been reported in DS brain tissue and shows further exacerbation with age27 while investigations in blood in DS with or without AD showed elevated levels of proinflammatory markers with a combined measure of amyloid‐β and inflammatory agents predicting future cognitive decline the following 24 months.56 Here, CD86 is linked to Alzheimer disease.