Besides the many relevations about Alzheimer’s that emerged at the World Alzheimer Congress 2000, still further leads are pouring off the scientific press. Investigators at the University of Virginia, for example, have just published a cell study in the August Annals of Neurology that suggests that abnormal mitochondrial DNA may be a culprit in sporadic (noninherited) forms of Alzheimer’s.

There is increasing evidence that Alzheimer’s disease is due to plaques in the brain, which in turn consist of beta amyloid protein, and that this protein in turn derives from an abnormal gene or genes involved in its production.

But where do these abnormal genes come from? In the some 10 percent of Alzheimer’s cases that are clearly familial, the abnormal genes are undoubtedly inherited as part of the DNA that is present in the nuclei of cells. But in the 90 percent of Alzheimer’s cases that are sporadic and presumably noninherited, the abnormal gene or genes may well come from DNA that is located in the mitochondria—those little energy powerhouses in the cell. And here’s the reason to think that this might be the case.

Neurologist James Bennett, Jr., M.D., and his colleagues at the University of Virginia Health System in Charlottesville took DNA from the platelet mitochondria of five persons with sporadic Alzheimer’s disease and from the platelet mitochondria of five neurologically healthy persons. They used the DNA to construct hybrid cells and then compared the cells containing DNA from the Alzheimer’s patients to that of cells containing DNA from the healthy controls. They found that the cells with DNA from the Alzheimer’s patients produced twice as much beta-amyloid protein as did the cells with DNA from the controls.

"For us, this is a major finding," Bennett said. "We show that a likely source of increased secretion and deposition of beta amyloid in the brains of Alzheimer’s disease patients derives from the defects in mitochondrial function induced by defective Alzheimer’s disease mitochondrial genes."