Researchers, including one of Indian-origin, have found that long-term antibiotic treatment in mice decreases levels of amyloid plaques, a hallmark of Alzheimer's disease.
Researchers, including one of Indian-origin, have found that long-term antibiotic treatment in mice decreases levels of amyloid plaques, a hallmark of Alzheimer’s disease.
The study, published in the journal Scientific Reports, 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.
“We’re exploring very new territory in how the gut influences brain health,” said senior author of the study Sangram Sisodia, Professor of Neurosciences at the University of Chicago.
Two of the key features of Alzheimer’s disease are the development of amyloidosis, accumulation of amyloid-beta peptides in the brain, and inflammation of the microglia, brain cells that perform immune system functions in the central nervous system.
For this study, Sisodia and his team administered high doses of broad-spectrum antibiotics to mice over five to six months.
At the end of this period, genetic analysis of gut bacteria from the antibiotic-treated mice showed that while the total mass of microbes present was roughly the same as in controls, the diversity of the community changed dramatically.
The antibiotic-treated mice also showed more than a two-fold decrease in amyloid-beta plaques compared to controls.
While the mechanisms linking these changes is unclear, the study points to the potential in further research on the gut microbiome’s influence on the brain and nervous system.
Sisodia cautioned that while the current study opens new possibilities for understanding the role of the gut microbiome in Alzheimer’s disease, it iss 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 noted.