Examining the interplay between cerebrovascular compromise and AD in the development of therapies is complicated by long prodromal phases of both conditions, necessitating preclinical studies. Four-month-old TgAD-F344 rats, which by six months of age present amyloid deposits and hyperphosphorylated tau, were treated with a nitric oxide synthase inhibitor L-NAME for one month to induce transient hypertension. Human umbilical cord perivascular cells were then given in combination with scyllo-inositol, an inhibitor of Abeta peptide oligomerization and fibrillization to elicit cerebrovascular repair and clear amyloid. Following L-NAME, non-transgenic rats showed transient cerebrovascular changes, whereas TgAD-F344 animals exhibited sustained increase in cerebrovascular reactivity. The latter effect was ameliorated by the treatment.