Stool transplantation can transfer symptoms of Alzheimer’s disease to a healthy young organism, as revealed by a recent study. This study is the first to show the causal role of the gut microbiota in Alzheimer’s disease.
Fecal microbiota transplantation
Renowned for their expertise in microbiota research, scientists from APC Microbiome Ireland undertook a study to comprehensively investigate the role of gut microbiota in Alzheimer’s. To achieve this, they gathered stool samples from both Alzheimer’s patients and age-matched healthy individuals. They transplanted these samples into microbiota-depleted young adult rats. The findings were striking: the rats receiving fecal microbiota from Alzheimer’s patients exhibited behavioral impairments related to both memory and mood consistent with Alzheimer’s disease.
Link between gut microbiota and cognitive health
These memory and mood impairments correlated with the cognitive scores of the donor patients, providing a clear link between gut microbiota, cognitive health, and Alzheimer’s symptoms. Furthermore, the researchers noticed changes in metabolites in both the rats’ intestines and hippocampi, suggesting biochemical changes caused by the transplantation. These findings suggest that changes in the gut microbiome of Alzheimer’s patients are not just a result of the disease but might also be the starting point of the disease itself.
Potential for probiotic intervention
The results of this study reveal that the makeup of our gut microbiota has a causal role in the development of Alzheimer’s disease. Considering the involvement of the gut microbiota in Alzheimer’s disease, future investigations may explore the impact of probiotics in combating this condition. While more research is needed, this groundbreaking study paves the way for achieving our shared objective; enhancing global quality of life through the provision of high -quality premium probiotics.
Grabrucker S, Marizzoni M, Silajdžić E, Lopizzo N, Mombelli E, Nicolas S, et al. Microbiota from Alzheimer’s patients induce deficits in cognition and hippocampal neurogenesis. Brain. 2023;awad303.
