Humanin and the receptors for humanin

Mol Neurobiol. 2010 Feb;41(1):22-8. doi: 10.1007/s12035-009-8090-z. Epub 2009 Dec 9.

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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

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

Substances

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