Humanin affects object recognition and gliosis in short-term cuprizone-treated mice. (December 2017)

• Record Type: Journal Article
• Authors: Murakami, Minetaka; Nagahama, Masatoshi; Abe, Yoichiro; Niikura, Takako
• Is Part Of: Neuropeptides. Volume 66(2017)
• Page Start: 90
• Page End: 96
• Publication Date: 2017-12
• Subjects: Humanin -- Cuprizone -- Neuroinflammation -- Amnesia; Neuropeptides -- Periodicals; Neuropeptides; Neuropeptides -- Périodiques; Neuropeptides; Electronic journals; Periodicals; 572.65
• DOI: 10.1016/j.npep.2017.10.002
• Languages: English
• ISSNs: 0143-4179

Abstract

Abstract: Humanin (HN) is a 24-residue peptide that manipulates cell survival under various stresses. A highly potent HN derivative, HNG, reduced amyloid burden and neuroinflammation and suppressed cognitive impairment in Alzheimer's disease model mice. Cuprizone (CPZ), a copper chelator, provokes demyelination in the central nervous system of mice. A shorter (one week) exposure to CPZ induces schizophrenia-like behavior and glial activation prior to demyelination. We tested the effect of HNG on these short-term responses to CZP in mice. Intraperitoneal injection of HNG for one week improved object recognition memory but not working memory in CPZ-treated mice. Quantitative PCR analyses showed that HNG significantly suppressed CPZ-induced activation of microglia, but did not alter the reduced level of a myelin-specific transcript. These results suggest that HN can suppress neuroinflammation and the associated cognitive deficit in a wider range of neurological disorders beyond Alzheimer's disease. Highlights: Short-term exposure to cuprizone induces amnesia and neuroinflammation in mice. Humanin improved object memory in cuprizone-treated mice. Humanin partially suppresses cuprizone-induced activation of glial cells. Humanin has no effect on cuprizone-induced downregulation of myelin-specific gene expression.