Groundbreaking study reveals gut microbiota’s causal role in Alzheimer’s 

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. 

Transplanting fecal microbiota

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. 

Link between gutmicrobiota and cognitive health

These 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 notable 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 study’s discoveries reveal the potential for probiotic intervention in the battle against Alzheimer’s. Furthermore, the results not only present new treatment possibilities but also emphasize the significance of maintaining a healthy gut microbiota for overall brain health. In essence, this research paves the way for achieving our shared objective of 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.