Antibiotics might fight Alzheimer’s plaques
Mouse study links drug-induced changes in gut bacteria to reduced A-beta buildup in brain
A long course of antibiotics reduced the levels of a hallmark of Alzheimer’s disease in the brains of mice, possibly by changing the species of bacteria in the gut. The results, described July 21 in Scientific Reports, suggest that gut bacteria may be linked in some way to Alzheimer’s.
The finding is preliminary, cautions neurobiologist Robert Moir of Massachusetts General Hospital, but it certainly merits more research. “It’s a nice new step in what could be a new strategy,” he says.
Recent studies that found links between microbes in the gut and the brain (SN: 4/2/16, p. 23) captured the attention of study coauthor Sangram Sisodia of the University of Chicago and colleagues. They wondered whether antibiotics could affect sticky globs of amyloid-beta, a protein that accumulates into plaques in the brains of people with Alzheimer’s. “We really didn’t know what to expect,” Sisodia says. “We did the experiment blindly.”
The researchers fed a cocktail of antibiotics to mice genetically engineered to develop A-beta plaques in their brains. Compared with mice that didn’t receive the drugs, mice that had received antibiotics for most of their lives had similar amounts of bacteria in their guts overall, but the species of bugs changed. Instead of hosting a wide variety of bacteria, the antibiotic-treated mice had a less diverse crowd.
This microbial shift in the gut appeared to affect the brain. Mice treated with antibiotics had fewer plaques in their brains than mice that didn’t receive the drugs. What’s more, the plaques that were there were smaller.
Sisodia and colleagues don’t know how bacteria signal from the gut to the brain to affect A-beta, although their study raises one possibility. Bacteria may send messages to the brain by changing the levels of immune system molecules carried in the blood. Antibiotics raised the levels of several such molecules, the researchers found.
Moir cautions that the results in mice might not apply to people. “It certainly looks promising, but it doesn’t mean that that’s what’s going to happen in humans.”
If a similar relationship between gut bacteria and Alzheimer’s does exist in people, that might allow new treatment options. “It’s way too early to think about antibiotics as a potential treatment or preventative measure for Alzheimer’s,” Sisodia says. But perhaps scientists can uncover new molecules that bacteria produce that could inhibit plaque formation in the brain.