Mild cognitive impairment (MCI) is an age‐related disorder that contributes to a reduced quality of life in older adults. However, the underlying mechanisms contributing to MCI with aging are incompletely understood. We tested the hypothesis that old C57 male mice demonstrate cerebrovascular endothelial dysfunction associated with MCI. Endothelium‐dependent dilation (EDD) (ex vivo dilation of mid cerebral and posterior communication arteries to acetylcholine [ACh]) was impaired in old (O: 22–26 mo, n= 17) vs. young (Y: 3–6 mo, n=11) mice (51.2 ± 5.9 % vs. 72.4 ± 5.4 %, p<0.05), and this was associated with reduced L‐NAME‐sensitive dilation (O: 16.1 ± 9.1 % vs. Y: 49.5 ± 9.5 %, p<0.05). Basal NO inhibition by L‐NAME had no effect on phenylephrine‐induced vasoconstriction in O (Con. 23.1 ± 2.8 % vs. L‐NAME 31.1 ± 4.1 %), but increased constriction in Y (Con 19.9 ± 3.1 % vs. L‐NAME 38.0 ± 3.9 %, p<0.05). O (n = 7) had impaired spatial learning during the Morris water maze test (p<0.05) and this was unrelated to differences in vision. In the probe trial, O had lower platform crossing numbers than Y (n =8) (O: 2.7 ± 0.5 vs. Y: 5.1 ± 0.7, p<0.05), suggesting O had impaired spatial memory compared to Y. These results indicate that cerebrovascular endothelial dysfunction, as reflected by reduced basal NO production and NO‐dependent EDD, develops with aging and is associated with MCI in C57 mice.Work supported by NIH AG013038 and AG000279.