The Baylor School of Medicine has provided an update on faculty research regarding fungal activity in the human brain and its involvement in the development of chronic neurodegenerative conditions. According to the press release, this research potentially contributes an important new piece of the puzzle regarding the development of Alzheimer's disease.
The current explanation for Alzheimer's disease is that it is primarily caused by the accumulation of toxic amyloid beta (Ab)-like peptides in the brain, leading to neurodegeneration. These peptides are believed to be produced endogenously, with the brain's own proteases breaking down amyloid precursor proteins to generate the toxic Ab peptides. However, the Baylor researchers propose that the brain Ab-peptide aggregates associated with multiple Candida-associated neurodegenerative conditions, including Alzheimer's disease and Parkinson's disease, may be generated both intrinsically by the brain and by the fungus Candida albicans (C. albicans).
Previous research conducted at Baylor College of Medicine revealed that C. albicans enters the brain by producing enzymes called secreted aspartic proteases (Saps), which break down the blood-brain barrier and allow the fungus to access the brain. Once inside the brain, C. albicans generates Ab-like peptides, which are considered toxic protein fragments and are believed to play a pivotal role in the development of Alzheimer's disease.
In a recent trial with laboratory mice, researcher David Corry, a professor of pathology and immunology and medicine at Baylor, demonstrated that it is possible to clear the fungal infection from the brain. The study showed that the Ab-like peptides also activate microglial cells in the brain, which help minimize the levels of fungi in the brain. However, this activation does not completely clear the infection.
Additionally, the researchers discovered that C. albicans produces a protein called candidalysin, which binds to microglial cells in the brain through a different receptor than the Ab-like peptides. This binding is also an essential part of clearing the brain from infection.
The findings from this research shed light on the complex relationship between fungal activity, Ab-like peptides, and neurodegenerative conditions such as Alzheimer's disease. Understanding these mechanisms could potentially lead to new therapeutic approaches for treating and preventing these chronic neurodegenerative conditions.
Further research is needed to fully understand the role of fungal activity in the development of Alzheimer's disease and other neurodegenerative conditions. However, this work from Baylor College of Medicine provides valuable insights and opens up new avenues for exploration in the field of neurodegenerative research.
