Abstract

Neuroprotective drugs tested in clinical trials, particularly those that block N-methyl-D-aspartate-sensitive glutamate receptors (NMDARs), have failed miserably in large part because of intolerable side effects. However, one such drug, memantine, was recently approved by the European Union and the US FDA for the treatment of dementia following our group's discovery of its clinically tolerated mechanism of action. Here, we review the molecular basis for memantine efficacy in neurological diseases that are mediated, at least in part, by overactivation of NMDARs, producing excessive Ca²⁺ influx through the receptor's associated ion channel and consequent free-radical formation.

Author affiliations

1. Burnham Institute for Medical Research, The Salk Institute for Biological Studies, The Scripps Research Institute, and the University of California at San Diego, 10901 North Torrey Pines Road, La Jolla, California 92037, USA.
   Email: slipton@burnham.org

Published online 20 January 2006

MORE ARTICLES LIKE THIS

These links to content published by NPG are automatically generated.