Humanin affects object recognition and gliosis in short-term cuprizone-treated mice.
Murakami. Minetaka M; Nagahama. Masatoshi M; Abe. Yoichiro Y; Niikura. Takako T
Key Findings
- HNG improved object recognition memory in cuprizone‑treated mice
- HNG significantly reduced microglial (brain immune cell) activation caused by cuprizone
- HNG did not change the lowered myelin‑specific gene expression or working memory performance
Practical Outcomes
- The results hint that humanin‑based peptides might protect against inflammation‑related memory loss, but the study is in mice, uses an experimental drug form, and lacks human dosing or safety data. Biohackers should view this as early‑stage evidence, not a ready‑to‑use protocol, and wait for more research before trying humanin supplements for brain health.
Summary
In mice that were given a chemical causing brain inflammation, a short‑term injection of a humanin‑derived peptide (HNG) helped them remember objects better and reduced the brain's inflammatory cells, though it didn’t improve other memory tasks or restore myelin levels.
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.
Study Information
pubmed
2017
2017-10-14T00:00:00.000Z
10.1016/j.npep.2017.10.002
13
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