Fungi drive many chronic health conditions, including asthma, skin problems, gut disorders, and others. Recent research has highlighted potential links between the fungus Candida albicans and Alzheimer’s disease. A recent study in mice found that C. albicans triggers a dual-pronged defense system involving both the brain and the immune system; however, when elements of this system fail, the fungi can impair the blood-brain barrier and drive amyloid plaque formation.
Researchers injected mice with different strains of C. albicans and measured fungal levels in the animals' brains. They assessed their immune responses and examined their transendothelial electrical resistance – a crucial measure of the integrity and functionality of the endothelial layer, which forms the blood-brain barrier.
They found that Candida albicans employed enzymes called aspartic proteinases (Saps) to compromise blood-brain barrier integrity, facilitating fungal entry into the brain. Interestingly, the presence of Saps promoted the breakdown of amyloid precursor protein (APP) into smaller, potentially protective components to combat the fungal invasion.
The fungi also released candidalysin, a toxin that contributes to Candida albicans virulence. When microglia (brain immune cells) recognized the altered APP components and candidalysin, they synergized their efforts, driving the eradication of the fungus from the brain. However, if the microglia failed to recognize the APP or candidalysin, the fungus persisted in the brain, eliciting damage to neuronal tissues.
Amyloid precursor protein occurs naturally in the body, particularly in brain tissues. It participates in various cellular functions, including forming and maintaining synapses, which are essential for communication between nerve cells. Abnormal APP processing can promote amyloid-beta accumulation, a hallmark of Alzheimer’s disease.
These findings suggest the brain employs a complex defense system to protect itself against Candida albicans, a common fungus. However, the system’s failure may drive amyloid-beta accumulation and possibly Alzheimer’s disease. Learn more about amyloid-beta in this clip featuring Dr. Dale Bredesen.
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