Other potential mechanisms are (1) the upregulated expression and/or activity of matrix metalloproteinases (MMPs), particularly MMP-2 and MMP-9, in the vessel wall as they are known to degrade arterial elastin, are linked to mild cognitive impairment and AD, and are activated by Aβ oligomers [10, 24, 35]; and (2) altered production of vascular smooth muscle-derived arterial elastin due to the change of a contractile to a proliferative vascular smooth muscle phenotype [30, 47]. Here, ELN is linked to Alzheimer disease.