Galanin protects against intracellular amyloid toxicity in human primary neurons.

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-beta (Abeta)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 Abeta 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.