New Research Suggests Common Fungi Can Penetrate Mammal Brain and Trigger Alzheimer’s-like Symptoms
Scientists have made a groundbreaking discovery that a common type of fungi, Candida albicans, has the ability to penetrate the mammal brain and trigger toxic amyloid plaques similar to those associated with Alzheimer’s disease. The findings, although conducted on mice, suggest that certain neurodegenerative conditions may originate from sources outside the brain.
Amyloid protein clumps, commonly found between neurons, have long been associated with Alzheimer’s disease and are believed to be the result of stress or inflammation within the brain. However, recent studies have shown the presence of this common fungus, Candida albicans, in the autopsied brains of individuals with Alzheimer’s and other neurodegenerative disorders.
These findings have led researchers at the Baylor College of Medicine in the United States to investigate further, this time focusing on mice. Previous studies conducted by the same lab at Baylor revealed that mice infected with Candida albicans experienced memory impairments, which resolved once the fungus was eliminated.
The new research delves into the molecular basis of this effect, primarily through “test-tube” experiments. Mice were injected with Candida albicans directly into their brains, and four days later, their brains were analyzed.
The findings indicate that Candida albicans, once in the brain, triggers two neuroimmune mechanisms. The first mechanism involves a fungal enzyme called Saps, which increases the leakiness of the blood-brain barrier, allowing fungal cells from the bloodstream to enter the brain. Simultaneously, Saps breaks down amyloid beta-like proteins, similar to those found in Alzheimer’s plaques, activating clean-up cells known as microglia.
The second mechanism involves another fungal secretion, which prompts microglia to target and remove the fungi. Together, these immune pathways effectively resolve Candida albicans infections in healthy mouse brains within approximately 10 days.
However, when the researchers disrupted the microglia response in mouse brains, the Candida albicans infections persisted for longer periods. This suggests that the presence of amyloid beta-like clumps may be harmful if not properly cleaned up by microglia.
The study aligns with recent findings indicating that amyloid beta plaques are not the initial triggers of cognitive decline in Alzheimer’s disease, thereby explaining the limited success of treatments targeting these plaques in humans.
Immunologist David Corry, who led the research at Baylor, believes this discovery contributes an important piece to the puzzle of Alzheimer’s disease development. He states that the prevailing belief is that the toxic amyloid beta peptides are produced endogenously in the brain. However, this study suggests that external factors, such as Candida albicans, could be responsible.
While further research is necessary, both on living animal models and human cells, the scientists at Baylor are hopeful that these initial findings may pave the way for innovative therapies for cognitive decline in the future. The study was published in Cell Reports.