Humanin and the receptors for humanin.

Abstract

Alzheimer's disease (AD) is a prevalent dementia-causing neurodegenerative disease. Neuronal death is closely linked to the progression of AD-associated dementia. Accumulating evidence has established that a 24-amino-acid bioactive peptide, Humanin, protects neurons from AD-related neuronal death. A series of studies using various murine AD models including familial AD gene-expressing transgenic mice have shown that Humanin is effective against AD-related neuronal dysfunction in vivo. Most recently, it has been shown that Humanin inhibits neuronal cell death and dysfunction by binding to a novel IL-6-receptor-related receptor(s) on the cell surface involving CNTFRalpha, WSX-1, and gp130. These findings suggest that endogenous Humanin [or a Humanin-like substance(s)] may suppress the onset of AD-related dementia by inhibiting both AD-related neuronal cell death and dysfunction.

• Authors: Masaaki Matsuoka, Yuichi Hashimoto
• Journal: Molecular neurobiology (Mol Neurobiol) Vol. 41 Issue 1 Pg. 22-8 (Feb 2010) ISSN: 1559-1182 [Electronic] United States
• PMID: 19997871 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)

Chemical References

• Amyloid beta-Peptides
• Intracellular Signaling Peptides and Proteins
• Membrane Proteins
• Nerve Tissue Proteins
• humanin

Topics

• Alzheimer Disease (metabolism, pathology)
• Amyloid beta-Peptides (metabolism)
• Animals
• Brain (metabolism, pathology)
• Cell Death (physiology)
• Humans
• Intracellular Signaling Peptides and Proteins (metabolism)
• Membrane Proteins (metabolism)
• Nerve Tissue Proteins (metabolism)
• Neurons (metabolism, pathology)