New Study Suggests Fungus Candida Albicans Could Play a Role in Alzheimer’s Disease Development
A recent study conducted by researchers from Baylor College of Medicine has shed light on the potential involvement of the fungus Candida albicans in the development of Alzheimer’s disease. The study, which utilized animal models, found that the fungus is able to breach the blood-brain barrier using enzymes and can produce toxic protein fragments known as amyloid beta (Ab)-like peptides, which are believed to be central to the development of Alzheimer’s.
Previous research has already linked fungi to chronic neurodegenerative conditions such as Alzheimer’s disease, but the mechanisms behind their involvement are not yet fully understood. In this study, the team of researchers from Baylor College of Medicine and collaborating institutions investigated how Candida albicans enters the brain and triggers processes that promote its clearance. Importantly, they also discovered that the fungus generates toxic protein fragments similar to those observed in Alzheimer’s disease.
Commenting on the findings, Dr. David Corry, the corresponding author of the study and a professor at Baylor College of Medicine, stated, “Our lab has years of experience studying fungi, so we embarked on the study of the connection between Candida albicans and Alzheimer’s disease in animal models.” He further explained, “In 2019, we reported that Candida albicans does get into the brain where it produces changes that are very similar to what is seen in Alzheimer’s disease. The current study extends that work to understand the molecular mechanisms.”
The researchers discovered that Candida albicans produces enzymes called secreted aspartic proteases (Saps) that break down the blood-brain barrier, allowing the fungus to access the brain and cause damage. Additionally, they found that two separate mechanisms activated by the fungus in brain cells called microglia effectively clear the fungus from the brain. The study revealed that the same enzymes used by the fungus to breach the blood-brain barrier also break down the amyloid precursor protein, leading to the production of Ab-like peptides. Furthermore, another protein produced by Candida albicans, called candidalysin, plays a crucial role in the clearance of the fungus from the brain.
Dr. Yifan Wu, the first author of the study, emphasized the significance of these findings, stating, “This work potentially contributes an important new piece of the puzzle regarding the development of Alzheimer’s disease.” The current understanding is that Alzheimer’s is primarily caused by the accumulation of toxic Ab-like peptides in the brain, which leads to neurodegeneration. However, the study suggests that both the brain and Candida albicans can generate these toxic protein fragments.
Dr. Corry highlighted the need for further research, stating, “These findings in animal models support conducting further studies to evaluate the role of Candida albicans in the development of Alzheimer’s disease in people, which can potentially lead to innovative therapeutic strategies.”
The study, titled “Toll-like receptor 4 and CD11b expressed on microglia coordinate eradication of Candida albicans cerebral mycosis,” was published on October 10, 2023, in the journal Cell Reports.