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Humanin

HN, S14G-Humanin

Quick Stats
Studies 491
Trials 100
Score 3
2006 pubmed

Colivelin prolongs survival of an ALS model mouse.

Chiba. Tomohiro T; Yamada. Marina M; Sasabe. Jumpei J; Terashita. Kenzo K; Aiso. Sadakazu S; Matsuoka. Masaaki M; Nishimoto. Ikuo I

Key Findings

  • Colivelin improved motor performance in ALS mice in a dose‑dependent way
  • Colivelin extended the lifespan of ALS mice compared with controls
  • Treated mice showed more surviving spinal‑cord motor neurons

Practical Outcomes

  • The result suggests humanin‑based peptides might protect nerve cells, but there’s no safe human protocol yet. Biohackers should treat this as early‑stage research and wait for clinical trials before considering any use.

Summary

A lab-made peptide called Colivelin, which includes a piece of the humanin protein, helped mice that model ALS live longer and move better, but this was only shown in mice and used direct brain injections, so it’s not something you can try now.

Abstract

Amyotrophic lateral sclerosis (ALS) is the most common motor neuron disease for which there is no sufficiently effective therapy. We have reported in our earlier study that intracerebroventricular (i.c.v.) injection of activity-dependent neurotrophic factor (ADNF) improves motor performance of G93A-SOD1 transgenic mice without significant prolongation in survival. Here, we found that i.c.v. injection of a synthetic hybrid peptide named Colivelin composed of ADNF and AGA-(C8R)HNG17, a potent derivative of Humanin that is a bioactive peptide with anti-Alzheimer's disease activity, dose-dependently improved motor performance and prolonged survival of ALS mice. Histological analysis, performed at the age of 120 days, demonstrated increased motoneuronal survival in spinal cords of Colivelin-treated mice as compared with saline- or ADNF-treated mice, indicating that Colivelin is a promising neurotrophic peptide for treatment of ALS.

Study Information

Provider

pubmed

Year

2006

Date

2006-03-10T00:00:00.000Z

DOI

10.1016/j.bbrc.2006.02.184