While preliminary, a growing body of evidence is linking fungal species with Alzheimer’s dementia. While less than one percent of all microorganisms that occupy the human body are fungal (the other 99% being bacterial or archaea), the nearly 400 species of fungi known to inhabit humans are looking like major players in human disease and aging. Fungi are known to populate the skin, mouth, nasal passages, throat, airway, vagina, and gastrointestinal tract. We now know that our brains are also home to fungal species. But are they contributors to diseases such as Alzheimer’s dementia and other neurological diseases such as amyotrophic lateral sclerosis (Lou Gehrig’s disease)?
Evidence is accumulating that fungal infestation of the human brain is indeed a factor in brain health and disease. Injecting a small quantity of Candida albicans into the bloodstream of experimental mice, for instance, and brain inflammation develops along with many of the hallmark signs of Alzheimer’s, such as accumulation of beta amyloid plaques. Numerous species of fungi have been recovered from the brains of people with dementia, especially Alternaria, Malassezia, and Candida albicans. Even more surprisingly, young people without dementia also harbor fungi in their brains, though not in as plentiful numbers as those with dementia, and fungal numbers in brain tissue increase with age: the older you are, the more your brain is occupied by fungal species. People with dementia also have higher blood levels of antibodies against various fungi, as well as higher blood levels of the fungal protein (1,3)-β-glucan, suggesting that fungi are not confined to the brain, raising the question whether fungal infection begins elsewhere in the body—gastrointestinal tract, sinuses, mouth—that then seed the brain with fungi.
Recent research has also uncovered the fact that beta amyloid, the material comprising the plaques that accumulate in dementia, exerts potent antimicrobial properties, most potently against Candida albicans, less potently against bacterial species such as E coli and Staphylococcus epidermis. This intriguing observation therefore raises the question: Is beta amyloid accumulation in dementia not a causal factor, but part of an immune response against pathogens, especially fungal pathogens?
The picture gets even more complicated: Fungal species such as Candida tropicalis may be inadequate to cause disease on its own but require the “cooperation” of bacterial species such as E. coli and Serratia marcesens that, in combination, are especially effective at forming an intestinal biofilm, making them less susceptible to the human immune system or antibiotics/antifungals and thereby better able to proliferate and cause intestinal diseases such as Crohn’s disease and/or serve as a repository to seed other parts of the body.
Of course, all of this cannot serve to prove that fungal species such as Malassezia or Candida tropicalis cause dementia and other brain diseases. Proof of a cause-effect association will need to come from a study in which people with Alzheimer’s dementia are treated with anti-fungal agents versus placebo and witnessing the effect on psychometric (memory, mental capacity) testing, imaging of hippocampal size, and other relevant disease measures. In the meantime, it is wise to be aware of the relationship of intestinal fungal overgrowth with conditions such as eczema, irritable bowel syndrome, inflammatory bowel disease, celiac disease, and autoimmune conditions and perhaps even take anti fungal action, such as the several strategies outlined in our Undoctored Inner Circle discussions about fungal overgrowth.