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Issue title: Drug Discovery for Neurodegenerative Diseases: Challenges and Novel Biochemical Targets
Guest editors: Gabriel B. Britton, Mark A. Smith, George Perry, Kumar Sambamurti and K.S. Jagannatha Rao
Article type: Review Article
Authors: Matsuoka, Masaaki; *
Affiliations: Department of Pharmacology, Tokyo Medical University, Tokyo, Japan
Correspondence: [*] Correspondence to: Masaaki Matsuoka, Department of Pharmacology, Tokyo Medical University, 6-1-1 Shinjuku, Shinjuku-ku, Tokyo160-8402, Japan. Tel: +81 3 3351 6141; Fax: +81 3 3352 0316; Email: [email protected].
Abstract: Despite a bulk of evidence supporting the idea that increased neurotoxic insults lead to Alzheimer's disease (AD), the possibility still remains that insufficiency of an endogenous defense system contributes to the disease progression. Humanin is a bioactive peptide that is likely to inhibit both neuronal death and dysfunction only related to AD by binding to a Humanin receptor on the cell-surface and by activating a STAT3-mediated signal, preventing the onset of dementia. A couple of recent studies presented evidence suggesting that the Humanin signal is decreased in neurons of AD patients. If this is the case, the restoration or activation of the Humanin signal in neurons may change the course of AD.
Keywords: Alzheimer's disease, Humanin, neuronal death, neuronal dysfunction
DOI: 10.3233/JAD-2011-102076
Journal: Journal of Alzheimer's Disease, vol. 24, no. s2, pp. 27-32, 2011
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