| Literature DB >> 19249060 |
Balpreet Matharu1, Gillian Gibson, Richard Parsons, Thomas N Huckerby, Susan A Moore, Leanne J Cooper, Robert Millichamp, David Allsop, Brian Austen.
Abstract
The ability of galantamine (Reminyl) to inhibit the aggregation and toxicity of the beta-amyloid peptide (Abeta) was investigated. Galantamine showed concentration-dependent inhibition of aggregation of both Abeta 1-40 and Abeta 1-42, as determined by an ELISA method. Electron microscope studies of Abeta 1-40 incubated in the presence of galantamine revealed fibrils that were disordered and clumped in appearance. MTT and lactate dehydrogenase assays, employing SH-SY5Y human neuroblastoma cells, showed that galantamine reduced the cytotoxicity induced by Abeta 1-40. Galantamine also dramatically reduced Abeta 1-40-induced cellular apoptosis in these cells. There is some evidence that galantamine may not be acting purely as a symptomatic treatment. Disease-modifying effects of the drug could be due to an additional effect on Abeta aggregation and/or toxicity.Entities:
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Year: 2009 PMID: 19249060 DOI: 10.1016/j.jns.2009.01.024
Source DB: PubMed Journal: J Neurol Sci ISSN: 0022-510X Impact factor: 3.181