Researchers from Lund University in Sweden have shown that intestinal bacteria can accelerate the development of Alzheimer’s disease. A new finding experts say could open the door to new opportunities for preventing and treating the disease.
According to the findings from the international collaboration between researchers from Food for Health Science Centre in Lund, and a research group from Ecole Polytechnique Federale de Lausanne in Switzerland: Our gut bacteria have a major impact on how we feel through the interaction between the immune system, the intestinal mucosa and our diet, thus, the composition of the gut microbiota is of great interest to research on diseases such as Alzheimer’s. Exactly how our gut microbiota composition is composed depends on which bacteria we receive at birth, our genes and our diet.
The study which was carried out on both healthy and diseased mice, shows that mice suffering from Alzheimer’s have a different composition of gut bacteria compared to mice that are healthy.
Researchers studied Alzheimer’s disease in mice that completely lacked bacteria to confirm the relationship between intestinal bacteria and the disease. Mice without bacteria had a significantly smaller amount of beta-amyloid plaque in the brain. Beta-amyloid plaques are the lumps that form at the nerve fibres in cases of Alzheimer’s disease.
In a test to clarify the link between intestinal flora and the occurrence of the disease, researchers discovered that germ-free mice developed more beta-amyloid plaques in the brain when given intestinal bacteria from diseased mice.
According to Frida Fåk Hållenius, associate professor at the Food for Health Science Centre
Our study is unique as it shows a direct causal link between gut bacteria and Alzheimer’s disease. It was striking that the mice which completely lacked bacteria developed much less plaque in the brain..
The results mean that we can now begin researching ways to prevent the disease and delay the onset, added Frida. We consider this to be a major breakthrough as we used to only be able to give symptom-relieving antiretroviral drugs.
Reference: T. Harach, N. Marungruang, N. Duthilleul, V. Cheatham, K. D. Mc Coy, G. Frisoni, J. J. Neher, F. Fåk, M. Jucker, T. Lasser & T. Bolmont. Reduction of Abeta amyloid pathology in APPPS1 transgenic mice in the absence of gut microbiota. Scientific Reports, 2017; 7: 41802 DOI: 10.1038/srep41802