Daniel M. Quinn, Ph.D.
University of Iowa
Iowa City, Iowa

2003 T. L. L. Temple Foundation Discovery Award

Deterioration in memory and problem-solving ability in Alzheimer’s disease are caused partly by depletion of the brain messenger chemical, or neurotransmitter, called acetylcholine. Current Alzheimer treatments temporarily increase available levels of acetylcholine by blocking the activity of cholinesterase, the chief enzyme that breaks down acetylcholine. All of these drugs are in the chemical class called cholinesterase inhibitors.

Daniel Quinn, PhD, and colleagues are working with newly developed, and possibly more potent, cholinesterase inhibitors. An emerging body of evidence suggests that cholinesterase may interact with amyloid plaques in a way that contributes to Alzheimer’s disease. This evidence raises the possibility that a new generation of more powerful cholinesterase inhibitors might not only stave off the cognitive losses associate with Alzheimer’s disease, but might also slow progression of the disease.