A COMMON microbe could help to trigger Alzheimer’s disease, say researchers in the US. If true, their controversial claim could turn the multimillion-dollar field of Alzheimer’s research on its head and force a rethink on how to prevent the disease.
The microbe in question is Chlamydia pneumoniae, which is spread by coughs and sneezes. By the age of 20, half the population has been infected with C. pneumoniae, and the likelihood of being infected increases with age. The bacterium has already been accused of triggering atherosclerosis-blocked arteries that can lead to heart attacks (“Can you catch a heart attack?”, New Scientist, 8 June 1996, p 38).
Alan Hudson at Wayne State University in Detroit and his colleagues did postmortems on the brains of 19 Alzheimer’s patients and 19 people of the same age who had died of other causes. They found signs of C. pneumoniae in 17 of the Alzheimer’s sufferers, in the hippocampus and temporal cortex. These are the parts of the brain which usually sustain most damage in Alzheimer’s disease. Unaffected areas of the brain were much less likely to harbor the bacterium. The bacterium turned up in the brain of only one of the non-Alzheimer’s patients. The team also managed to culture the microbe from two of the affected brains, showing that the organism was still alive rather than a long-dead bystander (Medical Microbiology and Immunology, vol. 187, p 23).
C. pneumoniae’s presence in the diseased brains does not mean that it cause Alzheimer’s, the scientists stress. But they think the bacterium may at least be a risk factor. Chlamydia bacteria do cause inflammation when they attack other parts of the body. And the brains of people with Alzheimer’s are inflamed and contain high levels of messenger chemicals called cytokines, which trigger inflammation.
Hudson says the bacterium infects microglia and astroglia, the cerebral cousins of scavenger cells called macrophages, and this produces inflammatory cytokines. “It seems reasonably likely that C. pneumoniae could be causing the inflammation,” says Hudson.
Source: New Scientist issue 15th August 1998, page 24
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