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Humanin

HN, S14G-Humanin

Quick Stats
Studies 491
Trials 100
Score 2
2016 pubmed 19 citations

Humanin ameliorates diazepam-induced memory deficit in mice.

Murakami. Minetaka M; Nagahama. Masatoshi M; Maruyama. Takuma T; Niikura. Takako T

Key Findings

  • S14G‑humanin reversed diazepam‑induced memory deficits in mice
  • It did not alter anxiety‑related behavior
  • It did not affect overall locomotor activity

Practical Outcomes

  • The result suggests humanin‑based compounds might one day be used to protect or restore memory under certain stressors, but there’s no evidence yet for safe or effective human use. Biohackers should view this as early‑stage science, not a ready‑to‑try supplement, and await human trials before considering any protocol.

Summary

A special form of the naturally occurring peptide humanin (called S14G‑humanin) helped mice recover memory that was blocked by the sedative drug diazepam, without changing their anxiety levels or movement. This shows the peptide can boost brain function in a specific drug‑induced situation, but the work is still only in animals.

Abstract

Humanin (HN) is an endogenous 24-residue peptide. A highly potent HN derivative, S14G-HN, which has a substitution of serine 14 to glycine, reduced amyloid burden and suppressed cognitive impairment in a mouse model of Alzheimer's disease. S14G-HN also suppressed amnesia induced by a muscarinic receptor antagonist in rodents. To understand the effects of HN on brain function, we tested the effect of S14G-HN on diazepam (DZP)-induced memory impairment and anxiety in mice using the object recognition test and zero-maze test, respectively. Intraperitoneal injection of S14G-HN reversed the DZP-induced memory deficit, whereas no significant change was observed in behavioral markers of anxiety. S14G-HN had no effect on locomotor activity in either test, indicating that S14G-HN did not affect physical functioning or motivation. These results suggest that HN preferentially influences cognitive function but not emotional function in the central nervous system.

Study Information

Provider

pubmed

Year

2016

Date

2016-10-29T00:00:00.000Z

DOI

10.1016/j.npep.2016.10.008

Citations

19

References

28