November 21, 1998

Microbe linked to Alzheimer’s disease

By J. Travis

Chlamydia pneumoniae is getting a bad reputation. Scientists first identified the bacterium a decade ago as the cause of severe, even fatal, respiratory failure in people. More recently, some investigators connected C. pneumoniae with atherosclerosis (SN: 6/14/97, p. 374). Now, a research group contends that this relatively common bacterium can invade the brain and perhaps trigger Alzheimer’s disease.

Although the origin of most cases of Alzheimer’s disease remains mysterious, scientists long ago ruled out infectious agents as suspects. Still, many researchers have amassed data suggesting that inflammation resulting from abnormal immune responses in the brain may lead to the cell death characteristic of the illness (SN: 12/5/92, p. 394). Moreover, anti-inflammatory drugs seem to slow the disease’s progression (SN: 2/19/94, p. 116).

Brian J. Balin of the Philadelphia College of Osteopathic Medicine and Alan P. Hudson of Wayne State University School of Medicine in Detroit wondered if C. pneumoniae sparks the brain’s aberrant immune response in Alzheimer’s disease.

The researchers found traces of the bacterium in the brains of 17 out of 19 people who had died with Alzheimer’s disease. In contrast, only 1 autopsied brain out of 18 from people without the illness had signs of the microbe, Balin and his colleagues reported at last week’s Society for Neuroscience meeting in Los Angeles. They also described the research in the August Medical Microbiology and Immunology.

Other scientists studying Alzheimer’s disease are intrigued by the new work but remain skeptical. "A bacterial infection in the brain could explain the widespread evidence of inflammation that one sees in Alzheimer’s brains," says Joseph Rogers of the Sun Health Research Institute in Sun City, Ariz. "We need to find out if this [finding] is a statistical fluke or true in many patients."

"Clearly, someone else is going to have to verify this information. On the surface, it’s difficult to believe," adds Paul Brown of the National Institute of Neurological Disorders and Stroke in Bethesda, Md., who many years ago unsuccessfully tried to transmit Alzheimer’s disease to monkeys by injecting tissue from diseased human brains.

The evidence of C. pneumoniae’s presence in the brain took several forms. Two tests detected DNA unique to the microbe. Antibodies that bind only to the bacterium stained regions of the brain affected in Alzheimer’s disease. Electron microscopy yielded pictures of C. pneumoniae in brain cells. Finally, the researchers grew the microbe from some of the brain tissue samples.

Unlike most bacteria, C. pneumoniae lives inside cells. While it hasn’t been found in the brain before, scientists could have mistaken the microbe for cellular structures known as lysosomes, argues Balin. Moreover, it infects brain cells called glia rather than the nerve cells that die in Alzheimer’s disease.

When glia are infected, they may produce immune molecules that ultimately harm neighboring nerve cells. "We think it’s the inflammation that’s really doing the damage," says Balin.

He and Rogers agree that it’s unclear how a bacterial infection produces the abnormal protein deposits typical of Alzheimer’s disease. One difficulty in evaluating the importance of C. pneumoniae’s presence in the brain, adds Rogers, is that pneumonia is the most common cause of death for people enfeebled by late-stage Alzheimer’s. "They may just be more susceptible to Chlamydia pneumoniae," he says.

From Science News, Vol. 154, No. 21, November 21, 1998, p. 325. Copyright © 1998 by Science Service.