Alzheimer’s disease: culpability of intestinal microbiota
Researchers have succeeded in "transmitting" symptoms of Alzheimer’s disease to juvenile rats, simply by transplanting the intestinal microbiota of patients with the disease. These microorganisms were enough to alter their spatial memory.
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About this article
Alzheimer’s disease is recognized as being multifactorial: genetics, lifestyle and environment are all involved. But according to a study published in the journal Brain 1 in October 2023, it seems that the intestinal microbiota also plays a role. And an important one at that: simply transplanting the intestinal microbiota of patients with Alzheimer’s disease into juvenile rats is enough to induce alterations in the animals' spatial memory, a typical symptom of the disease.
An unbalanced intestinal microbiota
It was already known that patients with Alzheimer’s disease have an altered intestinal microbiota. The authors reconfirm this observation, with, for example, a reduction in Coprococcus bacteria, associated with healthy aging, in patients.
The gut microbiota
But above all, they show that these changes are associated with the clinical condition of patients, and more specifically with their success in a test of cognitive and memory capacity called MMSE: the more certain bacteria recognized as beneficial to health are present, the higher the MMSE score; conversely, the abundance of deleterious bacteria (Desulfovibrio, for example) goes hand in hand with a deterioration in the MMSE score. Thus, intestinal bacteria are associated with patients’ cognitive performance.
A transfer of intestinal flora... and disease
But how do we understand this link between the gut and the brain? Does the intestinal microbiota contribute to Alzheimer’s disease, or is it also affected by the disease?
To answer this question, the team took stool samples from healthy donors and Alzheimer’s patients and transplanted them into young adult rats. The result: in rats that received the "Alzheimer’s" flora, the abundance of deleterious Desulfovibrio bacteria increases, the digestive system is altered (wetter stools, shortening of the colon, etc.) and, above all, the rats perform less well in exercises requiring their long-term spatial memory. In other words, symptoms comparable to those of humans affected by the disease.
Further experiments suggest that transplantation altered a process in these rats that enables them to produce new neurons. How can what happens in the digestive tract reach the brain? Probably via the bloodstream: an unbalanced intestinal microbiota produces small molecules capable of crossing the blood-brain barrier and jeopardizing neuroregeneration processes.
Of course, these are only preliminary results, which need to be confirmed by further studies. But they allow us to look at Alzheimer’s disease from a much broader angle than just the brain. Could this one day inspire new approaches aimed at delaying the onset or slowing the progression of dementia, or even neurodegenerative disorders and cognitive impairment in general?
