Researchers recently discovered that they could give young, healthy animals Alzheimer’s disease by transferring the gut microbiome of human subjects with Alzheimer’s into germ-free rats.
Published on Oct. 18 in Brain, the findings solidify that the microbiome—the collection of bacteria, viruses, and fungi that live mostly in the colon—has a role in the development of Alzheimer’s, the most common form of dementia, affecting 6.7 million Americans.
“This study represents an important step forward in our understanding of the disease, confirming that the makeup of our gut microbiota has a causal role in the development of the disease,” King’s College London neuroscience professor Sandrine Thuret, one of the study’s senior authors, said in a statement.
Our intestines are home to trillions of these microscopic bugs, which mostly live in symbiosis with the human body. Many factors, including antibiotics, glyphosate, medications, and stress, have been proven to kill beneficial microorganisms and cause an imbalance often referred to as dysbiosis.
Exactly what causes the microbial shift in people with Alzheimer’s disease is unclear.
“Bigger picture, it is likely that no one factor—food or lifestyle change—will, on its own, reduce the risk of developing cognitive decline as we age,” Percy Griffin, Alzheimer’s Association director of scientific engagement, said in a statement to The Epoch Times.
“Although this work is intriguing, it is still very preliminary. Larger studies in animal models and then in humans are required to make generalisations on what can be done in this area to reduce the risk of developing Alzheimer’s.”
There were 69 healthy control subjects and 64 Alzheimer’s patients in the study. Patients with Alzheimer’s had a higher abundance of inflammation-promoting bacteria in faecal samples, and these changes were associated with their cognitive status. Those traits were then found through a battery of behaviour tests in only the rats that were given transplants from Alzheimer’s patients.
“The memory tests we investigated rely on the growth of new nerve cells in the hippocampus region of the brain. We saw that animals with gut bacteria from people with Alzheimer’s produced fewer new nerve cells and had impaired memory,” lead author professor Yvonne Nolan said.
Alzheimer’s disease’s link to the microbiome has already been explored in recent studies, although it’s been largely unclear whether the disease caused the dysbiosis or if—as this research indicates—alterations in the intestinal community cause symptoms of dementia.
Mr. Griffin, who holds a doctorate in molecular cell biology from Washington University in St. Louis, noted that studies in rats don’t always indicate that similar findings will occur in the human body. To build credibility, the research needs to be replicated, he said.
“This is an interesting study that adds to our growing understanding of how the bacteria in the gut may contribute to the risk of Alzheimer’s disease. But this study is in rats, and rats are not people,” he said. “That said, these findings demonstrate a possible role for gut bacteria in affecting the areas of the brain that are (a) associated with memory and (b) involved in Alzheimer’s disease.”