Article ID Journal Published Year Pages File Type
1915150 Journal of the Neurological Sciences 2009 10 Pages PDF
Abstract

The ability of galantamine (Reminyl®) to inhibit the aggregation and toxicity of the β-amyloid peptide (Aβ) was investigated. Galantamine showed concentration-dependent inhibition of aggregation of both Aβ 1-40 and Aβ 1-42, as determined by an ELISA method. Electron microscope studies of Aβ 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 Aβ 1-40. Galantamine also dramatically reduced Aβ 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 Aβ aggregation and/or toxicity.

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