Study summary · research use only
Humanin and the receptors for humanin
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
This review discusses Humanin and its receptors in the context of Alzheimer's disease (AD). The authors describe AD as a prevalent dementia-causing neurodegenerative disease in which neuronal death is closely linked to progression of dementia, and state that accumulating evidence has established that a 24-amino-acid bioactive peptide, Humanin, protects neurons from AD-related neuronal death. They report that studies using various murine AD models, including familial-AD-gene-expressing transgenic mice, have shown Humanin to be active against AD-related neuronal dysfunction in vivo, and that Humanin was shown to inhibit neuronal cell death and dysfunction by binding a novel IL-6-receptor-related receptor involving CNTFRalpha, WSX-1, and gp130. The authors suggest that endogenous Humanin or a Humanin-like substance may suppress the onset of AD-related dementia by inhibiting both AD-related neuronal death and dysfunction.
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.
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