Affiliations: [a] Laboratory of Neurobiology and State Key Laboratory of Biomembrane and Membrane Biotechnology, College of Life Sciences, Peking University, Beijing, China | [b] Max-Planck Institute of Immunobiology, Freiburg, Germany | [c] CAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences, Beijing, China
Correspondence:
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Corresponding authors: Yan Zhang, Ph.D., Long-Chuan Yu, M.D., Ph.D. and George F. Gao, Ph.D., College of Life Sciences, Room 219, Peking University, Beijing, 100871, China. Tel.: +86 10 62754880; Fax: +86 10 62751526; E-mails: yanzhang@pku.edu.cn; yulc@pku.edu.cn; gaof@im.ac.cn.
Abstract: Galanin and galanin receptors are upregulated in the brain regions associated with Alzheimer's disease (AD). However, the consequence of this overexpression is still unknown, particularly in human neurons. Here, we investigate the possible protective effects of galanin against intracellular amyloid-β (Aβ)1–42 toxicity, as well as other insults including staurosporine, etoposide, hydrogen peroxide, and serum depletion in cultured human primary neurons. The results show that galanin is protective against intracellular Aβ cytotoxicity and all of the above insults at sub-nanomolar physiological concentrations. The galanin protection may be mediated by galanin receptor 2 and down-regulation of Bax level. The data from the present study provide a potential drug target for therapy or prevention of neurodegenerative diseases, including AD.
Keywords: Alzheimer's disease, galanin, human primary neurons, neuronal loss
