A new study in the Journal of Alzheimer’s Disease reveals a seemingly robust link between the neurogenerative illness and compounds released by gut bacteria. According to the study authors, these findings provide “indisputable” evidence that the intestinal microbiota plays a significant role in the development of Alzheimer’s.
The so-called gut-brain axis has been the subject of much scientific investigation and debate in recent years, with an increasing amount of data indicating that the microscopic inhabitants of our entrails directly influence our central nervous system. This two-way channel of communication allows the brain to send chemical messages to the gut in order to control appetite and digestion, while it is thought that the bacteria therein release a range of metabolites that impact brain function.
This had led to speculation that the make-up of a person’s microbiome could contribute to their likelihood of developing Alzheimer’s disease, although this link has never been confirmed. In an attempt to put the debate to bed, the authors of the new study recruited 89 volunteers between the ages of 65 and 85, some of whom were healthy while others suffered from varying degrees of cognitive decline. Using positron emission tomography (PET), the team scanned participants’ brains for signs of amyloid plaques, which are a key indicator of Alzheimer’s, while also collecting blood samples in order to search for gut bacteria metabolites.
Results indicated that those with more amyloid plaques in their brains tended to have higher levels of lipopolysaccharides in their blood. Found on the outer membrane of certain bacteria, these molecules are known to stimulate the formulation of amyloid plaques while also increasing inflammation in the brain. Similarly, short-chain fatty acids such as acetate and valerate were found to be elevated in the blood of those suffering from Alzheimer’s. Both of these are released by certain gut bacteria and have been associated with inflammation in the brain.
Other compounds that are known to interfere with endothelial cells and disrupt the integrity of the blood-brain barrier were also present in larger concentrations in people with high levels of amyloid plaques, indicating that this may represent another avenue by which gut microbiota influence the development of the disease.
In contrast, lower levels of amyloid plaques were correlated with higher concentrations of a short-chain fatty acid called butyrate, which is known to protect neurons by reducing inflammation in the brain.
In a statement, study author Moira Marizzoni claimed that these “results are indisputable: certain bacterial products of the intestinal microbiota are correlated with the quantity of amyloid plaques in the brain.”
However, while the confirmation of a link between gut bacteria and dementia is significant, co-author Giovanni Frisoni insists that “we shouldn’t be too quick to rejoice,” as this knowledge is unlikely to lead to a cure for neurodegenerative diseases. Instead, it could enable more effective identification of individuals who are at risk of developing such a condition, allowing for earlier interventions.
“We must first identify the strains of the [bacterial] cocktail,” he says. “Then, a neuroprotective effect could only be effective at a very early stage of the disease, with a view to prevention rather than therapy.”