Antibiotics may be a key to stopping the relentless progression of Alzheimer's disease. Neuroscientists at the University of Chicago found that long-term treatment with antibiotics decreases levels of mind-robbing plaques.
The study, which was conducted in mice, also showed significant changes in the gut microbiome after antibiotic treatment, suggesting the composition and diversity of bacteria in the gut play an important role in regulating immune system activity that impacts progression of Alzheimer's disease.
Two of the key features of Alzheimer's disease are the accumulation of amyloid-ß (Aß) plaques in the brain, and inflammation of the microglia, brain cells that perform immune system functions in the central nervous system. The severity of inflammation in the brain is believed to influence the rate of cognitive decline from the disease.
For the study, high doses of broad-spectrum antibiotics were administered to mice over five to six months. At the end of this period, genetic analysis of gut bacteria from the mice treated with antibiotics showed that while the total numbers of microbes in the gut were roughly the same as in controls, their diversity changed dramatically.
The antibiotic-treated mice also showed more than a two-fold decrease in Aß plaques compared to controls, and a significant elevation in the inflammatory state of microglia in the brain. Levels of important signaling chemicals circulating in the blood were also elevated in the treated mice.
While the scientists don't understand the mechanisms linking these changes, the study points to the potential in further research on the gut microbiome's influence on the brain and nervous system.
"We don't propose that a long-term course of antibiotics is going to be a treatment — that's just absurd for a whole number of reasons," said the study's lead author Myles Minter, Ph.D. "But what this study does is allow us to explore further, now that we're clearly changing the gut microbial population and have new bugs that are more prevalent in mice with altered amyloid deposition after antibiotics."
"We're exploring very new territory in how the gut influences brain health," said the study's senior author Sangram Sisodia, Ph.D. "This is an area that people who work with neurodegenerative diseases are going to be increasingly interested in, because it could have an influence down the road on treatments."
Sisodia cautioned that while the current study opens new possibilities for understanding the role of the gut microbiome in Alzheimer's disease, it's just a beginning step.
"There's probably not going to be a cure for Alzheimer's disease for several generations, because we know there are changes occurring in the brain and central nervous system 15 to 20 years before clinical onset," he said.
"We have to find ways to intervene when a patient starts showing clinical signs, and if we learn how changes in gut bacteria affect onset or progression, or how the molecules they produce interact with the nervous system, we could use that to create a new kind of personalized medicine," he concluded.
The study was published in Scientific Reports.
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