= 15, HF-PNA5 at 50 g/ kilogram body weight/day (HF-P50) n = 15.

= 15, HF-PNA5 at 500 g/ kilogram body weight / day (HF-P500) n Animal treatment groups were as listed: heart failure (HF)-saline treated n = 15, (HF-Saline), Sham surgery-saline treated n = 15 (Control-Saline), HF-Ang-(1-7) at 500 g/ kilogram body weight/ day for 24 days (HF-A500) n Within the last 3 days of injections, animals underwent Novel Object Recognition (NOR) testing (Fig. Mice recovered for 5 weeks following MI before receiving 24 days of daily subcutaneous drug treatment. Mice were assigned randomly to the following treatment groups: Control-Saline (sham MI surgery, treated with saline), HF-treated (HF-PNA5, or HF-Ang-(1-7) with either 50 g/kg/day, or 500 g/kg/day), or HF-saline. We have previously shown that PNA5 targets MasR, reverses cognitive impairment in our preclinical VCID model, and inhibits circulating and brain inflammatory cytokine production. Our collaborative team has developed and optimized a novel, synthetic Ang-(1-7)-derived glycopeptide, PNA5, that selectively activates MasR and has improved bioavailability and brain penetration compared to the native Ang-(1-7) peptide. MasRs that regulate vasodilation are highly expressed in the hippocampus and perirhinal cortex, which makes them an ideal target for treating brain disease related to hypoxia and inflammation that impair memory, such as VCID and ADRD.

Through targeting Mas receptors (MasR), located on neurons, microglia, and vascular endothelial cells in the brain, Ang-(1-7) decreases brain inflammation and increases cerebral circulation. Angiotensin 1-7 (Ang-(1-7)) is a clinically safe peptide that decreases inflammation and increases cerebral blood flow in our VCID preclinical model.

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