Mitochondria as Sensors of Amyloid‐Beta Toxicity and Regulators of Inflammation in Cerebrovascular Endothelial Cells

Deficits in mitochondrial function and metabolism were associated with Aβ but not Hcy, and accompanied by the release of mtROS, a mitochondria damage associated molecular patterns (mtDAMP). This, in turn, was associated to an increase in EC inflammatory markers and barrier permeability. Overall, our results reveal a novel role for mtDAMPs in vascular dysfunction in the presence of Aβ and/or Hcy.