Recent research suggests that the beta amyloid plaques found in the brains of Alzheimer sufferers may not be the primary cause of the disease. The immune system makes use of “clumping” of beta amyloid proteins to encapsulate various kinds of microbes which are deemed hostile to the body.
A few types of microbes are able to penetrate the blood-brain barrier, and may be causing low-grade, symptom-free infections. When the immune system responds by clumping beta amyloid protein around the invaders, the undesired side-effect of the proliferation of these encapsulating plaques are injurious to nerve tissue, and in sufficient quantity or disadvantageous concomitant conditions in the brain ecology, they lead to the progressive dementia of Alzheimer’s disease.
Focused research on the effect of the gut microbiome on the brain has only begun in the last few years, and new projects just now beginning to receive significant funding. Other microbiome research suggests that age-related changes in the oral microbiome may also contribute to Alzheimer’s disease.
Scientists are also studying the interaction between the gut microbiome and the permeability of the blood-brain barrier (BBB), which protects the brain from invasive microbes that may turn out to be a primary cause of Alzheimer’s. Recent studies show that the gut bacteria can cause the blood-barrier to become more permeable to unwanted substances, such as microbes. This could lead to the following sequence of events: increased risk for infection, activation of the brain’s immune system, and the resulting deposit of beta-amyloid plaque found in the brains of Alzheimer’s patients.
One study also has shown that intestinal bacteria can accelerate the development of Alzheimer’s disease in mice. Intestinal bacteria was transferred from diseased mice to germ-free mice, with the result that the mice developed more beta-amyloid plaques in the brain compared to controls.
Braniste, VA et al., The gut microbiota influences blood-brain barrier permeability in mice. Science translational medicine. 2014; 6(263):263ra158
Harach, T et al., Reduction of Abeta amyloid pathology in APPPS1 transgenic mice in the absence of gut microbiota. Scientific Reports, 2017; 7: 41802 DOI: 10.1038/srep41802