Study summary · research use only
AngIV-Analog Dihexa Rescues Cognitive Impairment and Recovers Memory in the APP/PS1 Mouse via the PI3K/AKT Signaling Pathway
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
In this study using APP/PS1 mice, an Alzheimer's disease model, different doses of the AngIV-analog Dihexa were administered orally. The abstract reports Dihexa crossed the blood-brain barrier, increased tissue angiotensin IV (Ang IV) levels compared to wild-type mice, and was associated with restored spatial learning and cognitive performance in the Morris water maze test. Dihexa was linked to increased neuronal cell numbers and SYP protein expression on Nissl staining, decreased astrocyte and microglia activation, reduced levels of the pro-inflammatory cytokines IL-1β and TNF-α, and increased levels of the anti-inflammatory cytokine IL-10. Dihexa activated the PI3K/AKT signaling pathway, and the PI3K inhibitor wortmannin reversed the anti-inflammatory and anti-apoptotic effects observed, according to the study.
Abstract
The renin-angiotensin system (RAS) is a paracrine RAS within the central nervous system (CNS) and is closely related to Alzheimer's disease (AD). The endogenous hexapeptide angiotensin IV (Ang IV), an important component of the brain RAS, was found to rescue cognitive impairment and recover memory in previous studies. In our study, we used different doses of Dihexa, which can be orally administered and cross the BBB in APP/PS1 mice. We found that the amount of AngIV in mouse tissue increased after the administration of Dihexa compared to that in the WT group. Meanwhile, Dihexa restored spatial learning and cognitive functions in the Morris water maze test. Dihexa increased the neuronal cells and the expression of SYP protein in APP/PS1 mice in Nissl staining. Furthermore, Dihexa decreased the activation of astrocytes and microglia, markedly reduced levels of the pro-inflammatory cytokines IL-1β and TNF-α and increased the levels of the anti-inflammatory cytokine IL-10. Dihexa activated the PI3K/AKT signaling pathway, while PI3K inhibitor wortmannin significantly reversed the anti-inflammatory and anti-apoptotic effects of APP/PS1 mice. These findings highlight the brain AngIV/PI3K/AKT axis as a potential target for the treatment of AD.
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