Fungal Infections in The Brain May Cause Alzheimer’s-Like Symptoms
Alzheimer’s disease, a progressive and irreversible brain disorder, affects millions of people worldwide, causing memory loss, cognitive decline, and behavioral changes. While the exact cause of Alzheimer’s remains unknown, a recent study has suggested a surprising link between fungal infections in the brain and the development of Alzheimer’s-like symptoms.
The study, published in the journal Scientific Reports, found that the presence of fungal infections in the brain significantly increased the risk of developing Alzheimer’s disease. Researchers examined post-mortem brain tissue samples from Alzheimer’s patients and found the presence of several fungal species, including Candida and Torulaspora. These fungi were found to be highly concentrated in the areas of the brain commonly affected by Alzheimer’s, such as the hippocampus and frontal cortex.
Furthermore, the researchers also observed that the toxins produced by these fungi were associated with the accumulation of amyloid plaques and neurofibrillary tangles, two distinct hallmarks of Alzheimer’s disease. These toxic byproducts induce inflammation and damage brain cells, leading to the characteristic symptoms of Alzheimer’s.
While this study provides strong evidence supporting the involvement of fungal infections in the development of Alzheimer’s, more research is needed to fully understand the relationship between the two. It is unclear whether these fungi act as primary causes of Alzheimer’s or exacerbate its progression in individuals already at risk.
Nevertheless, these findings open up new possibilities for the prevention and treatment of Alzheimer’s disease. Developing antifungal treatments or vaccines targeting the fungi involved could potentially halt or even reverse the progression of the disease. Additionally, identifying individuals at high risk of fungal infections in the brain may lead to the implementation of early interventions for Alzheimer’s prevention.
In conclusion, this groundbreaking study has shed light on the potential role of fungal infections in the development of Alzheimer’s disease. Further research in this area will undoubtedly deepen our understanding of the causes and mechanisms behind this devastating condition, paving the way for new treatments and prevention strategies.
A common type of fungus has now been shown to invade the brains of mammals and cause toxic amyloid plaques, such as those associated with Alzheimer’s disease.
The findings were made in mice, but the research suggests that a key feature of some neurodegenerative diseases could come from sources outside the brain.
Amyloid protein clumps that appear between neurons are strongly associated with Alzheimer’s disease and are widely believed to result from intrinsic stress or inflammation in the brain.
However, in recent years, scientists have discovered signs of a common fungus known as Candida albicans, in the autopsy of the brains of people with Alzheimer’s disease and other neurodegenerative disorders, such as Parkinson’s.
This has led some to argue that external infections can enter the mammalian brain and trigger an innate immune response, which can help destroy pathogens but can also cause Alzheimer’s-like symptoms if things go wrong.
To explore that idea further, an international team of researchers, led by experts from the Baylor College of Medicine in the United States, turned to mice.
Previously, the same laboratory at Baylor discovered that mice were infected with C. albicans showed disturbances in memory, but these disappeared when the fungus disappeared.
Now their new research investigates the molecular basis of that effect, mostly through ‘test tube’ experiments.
First, researchers injected C. albicans directly into the brains of mice. Four days later, the mice were euthanized and their brains were used for further analysis.
Several brain slices were imaged and some cells were grown on plates.
The findings suggest that oin the brain, C. albicans can activate two neuroimmune mechanisms, one that activates immune cells that suppress the fungi, and another that prompts them to eliminate the invader altogether.
The first mechanism involves a fungal enzyme called Saps, which makes the blood-brain barrier extra leaky. This allows fungal cells that may travel through the body’s bloodstream to the brain.
At the same time, Saps also breaks down amyloid beta-like proteins, similar to the proteins that form plaques in Alzheimer’s brains, which in turn activate cleanup cells called microglia.
The second mechanism involves another fungal secretion, which also triggers microglia, this time to target the fungi for removal.
Together, both immune pathways are ‘very effective in solving acute problems C. albicansinfections in the brains of healthy mice, usually within about 10 days.
But not all brains are young and healthy. When researchers purposefully disrupted the microglia response in mouse brains, they discovered that C. albicans infections lasted significantly longer.
“If we take away this pathway, fungi are no longer effectively removed from the brain,” says Yifan Wu of the Baylor College of Medicine.
The amyloid beta-like clumps found in the brains of mice appear to be sentinels against pathogen invasion, but if these clumps are not properly cleared by microglia, it is possible that their presence could be harmful in the long term.
That’s just a hypothesis for now, but it is consistent with recent findings indicating that amyloid beta plaques are latecomers in Alzheimer’s disease, rather than the original triggers of cognitive decline.
This could be why treatments that target these plaques in humans usually prove unsuccessful.
“This work may contribute an important new piece of the puzzle regarding the development of Alzheimer’s disease,” said immunologist David Corry, who led the research at Baylor.
“The dominant thought is that these peptides are produced endogenously. Our own brain proteases break down the amyloid precursor proteins that generate the toxic amyloid beta peptides.”
But that may not be the case after all.
Much more research needs to be done, both in living animal models and human cells, but Baylor researchers are hopeful that their initial experiments could lead to innovative therapies for cognitive decline in the future.
The research was published in Cell reports.
