Alzheimer's disease: source searching.

Using brain tissue taken from living patients, British researchers have been able to get one step closer to determining the initial biochemical changes that occur in Alzheimer's disease.

The memory loss and other cognitive disorders of Alzheimer's disease are all too evident to victims and their families; the current research, reported in the July 6 NEW ENGLAND JOURNAL OF MEDICINE, relates the psychological effects to decreased production of the chemical acetylcholine, a neurotransmitter that is involved in memory.

The role of acetylcholine was suspected as a result of autopsy studies, and because the neurotransmitter is involved in memory. This research represents the first "live" demonstration of the connection, Alzheimer's disease researcher Joseph T. Coyle of Johns Hopkins University in Baltimore told SCIENCE NEWS. In rare instances brain biopsies are done to confirm a diagnosis, and the researchers, from the University of London and other institutions, studied tissue collected over about five years from 17 patients. They incubated the brain cells with a radioactive precursor of acetylcholine, and found the cells were producing less than cells from apparently normal tissue removed from brain tumor patients. The more serious the outward manifestations of Alzheimer's disease, the less acetylcholine produced.

In autopsy studies of other patients, they found that changes in other neurotransmitter systems did not correlate as neatly to previously collected psychological data, leading them to conclude that damages to the other systems are not primary events in the disease.

The finding represents bad news and good news in terms of therapy. Because the "production machinery" and not the presence of raw materials seems to be at fault, current efforts to supply an acetylcholine precursor may be inappropriate, says Neil R. Sims, a researcher on the project who now works at the Burke Rehabilitation Center in White Plains, N.Y. But the finding that acetylcholine changes occur early in the course of the disease suggests that some other way of manipulating the metabolic pathway may be worthwhile, he says.