Food For Thought

Researchers have found that people with Alzheimer’s disease have more undesirable bacteria in their gut microbiome (the collection of bacteria, viruses, fungi, and other microbes that live in the gut), with less abundant amounts of beneficial bacteria like Bifidobacteria.

The authors of “Gut microbiome alterations in Alzheimer’s disease,” add Alzheimer’s disease to the growing list of diseases associated with gut microbial alterations. The findings from an article in Nature suggest that gut bacterial communities may be a target for therapeutic intervention.

Another study also found a distinctly different composition of bacteria in Alzheimer’s disease patients. The researchers conclude that alterations in gut microbial communities in Alzheimer’s disease patients may result in brain changes. They note that an abundance of Bacterioides (a type of bacteria) may cause inflammation that contributes to Alzheimer’s disease pathology.

A growing body of research supports this link between gut composition and brain inflammation. Scientists link intestinal microbiota to the inflammation found in various neurological conditions, including autism spectrum disorders, multiple sclerosis, Parkinson’s disease, and Alzheimer’s disease in an article in the Journal of Experimental Medicine.

Authors of an article in Smithsonian Magazine sum up these findings: “The microbes in the gastrointestinal tract influence the immune system and the brain, possibly playing a role in the development of Alzheimer’s.”

Dietary Inulin alters the gut microbiome, enhances systemic metabolism and reduces neuroinflammation in an APOE4 mouse model


In this study, a dietary intervention with inulin, a prebiotic, can effectively alter the gut microbiome in a preclinical Alzheimer’s Disease mouse model, enhance systemic metabolic functions and reduce brain inflammation characteristic of early Alzheimer’s Disease. They focused on the underlying metabolic features contributed by the APOE ε4 genotype, the largest risk factor for the development of Alzheimer’s Disease, and showed how dietary inulin intervention can mitigate them.

This represents a shift in Alzheimer’s Disease research, from the amyloid hypothesis to the metabolic features underlying the disease. As impairment of energy metabolism and elevation of neuroinflammation are well-established features of Alzheimer’s Disease, a prebiotic-rich diet might be a potentially useful approach to prevent the onset of the disease.

For future studies, it will be important to establish whether an inulin-enriched diet can inhibit Aβ aggregation and impede cognitive decline in symptomatic E4FAD mice. Understanding the dietary effects in the context of the gut-brain axis may have significant future implications for preventing Alzheimer’s Disease in asymptomatic APOE4 carriers.



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