Investigating the Connection Between Pathogens and Alzheimer’s Disease
A small yet determined group of researchers is diving into a potentially groundbreaking area of study: the link between infections and Alzheimer’s disease. This exploration seeks to uncover whether pathogens could be a contributing factor to this debilitating condition. The search for causal evidence is gaining momentum, especially in light of recent findings that suggest a possible connection.
The Research Landscape
This week, Philadelphia hosts the largest international conference dedicated to Alzheimer’s disease. Amidst this gathering, a smaller group of about 80 scientists is focusing on a niche yet crucial aspect: the potential role of pathogens in causing Alzheimer’s. This alternative meetup highlights the increasing interest in exploring connections beyond the widely accepted amyloid beta hypothesis, which posits that the plaque-forming brain protein drives the disease.
Momentum from the COVID-19 Pandemic
The COVID-19 pandemic has lent significant momentum to this field of study. The neurological symptoms experienced by some individuals with Long COVID have reinforced the notion that viruses can chronically disrupt brain function. This has led researchers to delve deeper into how infections might influence Alzheimer’s disease.
Emerging Evidence
Recent studies have uncovered evidence that infections can mobilize tau, a signature protein of Alzheimer’s. Additionally, a vaccine against shingles—a disease caused by a virus that remains in the nervous system—has been associated with a reduced risk of dementia. These findings suggest a potential protective response triggered by pathogens.
Key Findings and Studies
In 2016, Harvard University neuroscientist William Eimer and his mentor Robert Moir discovered that amyloid beta might protect against infection in mouse and worm models of Alzheimer’s disease. This finding suggested that pathogens could play a role in mobilizing the protein. Further evidence came in 2018, showing that amyloid beta aggregates in the presence of herpes simplex virus-1 (HSV-1).
In 2019, another team found Porphyromonas gingivalis, a bacterium causing gum disease, in the brains of Alzheimer’s patients. This bacterium triggered Alzheimer’s pathology in mice when applied to their gums. Additionally, research in 2020 demonstrated that HSV-1 could induce Alzheimer’s-like changes in a 3D stem-cell-derived tissue culture.
The Role of Pathogens in Alzheimer’s
Animal studies continue to build the case. At Baylor College of Medicine, researchers found yeast cells in the brains of mice infected with Candida albicans, leading to increased anxiety, memory problems, and brain shrinkage. These findings support the hypothesis that pathogens could contribute to Alzheimer’s pathology.
Eimer’s team has also shown that when human neuronal cells are exposed to HSV-1, another protein, tau, congregates and offers protection. This suggests that tau, like amyloid beta, might be an antimicrobial protein. Their ongoing research aims to establish a more definitive link between infections and Alzheimer’s.
Human Studies and Epidemiological Evidence
Human studies are also contributing to this field. A recent analysis of health records from over 200,000 people in the U.S. found that those who received the shingles vaccine Shingrix had a 17% lower risk of dementia. A separate study in Wales showed a 20% reduction in dementia risk for those who received an earlier shingles vaccine. These findings bolster the argument that infections might influence Alzheimer’s risk.
Overcoming Challenges and Future Directions
Despite the accumulating evidence, establishing a direct causal link between pathogens and Alzheimer’s in humans remains challenging. Lon Schneider, director of the California Alzheimer’s Disease Center, emphasizes the need to move beyond associations to prove causality. This is the primary goal of the Alzheimer’s Pathobiome Initiative (AlzPI), which encourages collaboration and data sharing among researchers.
AlzPI co-founder Brian Balin and his team believe that repeated infections might be necessary to trigger Alzheimer’s. Pathogens that can remain latent and reactivate, such as herpesviruses, could be particularly harmful. Researchers at Tulane University are investigating this by mimicking the cycle of active infection and latency in mice, revealing significant brain changes after repeated infections.
Testing Antimicrobial Treatments
Some teams are already exploring antimicrobial treatments for Alzheimer’s. Columbia University is leading a trial of the herpes antiviral valacyclovir, and Lighthouse Pharma is raising funds for a study on a drug that inhibits P. gingivalis. Although earlier trials faced challenges, they showed potential effectiveness in certain cases.
Conclusion
The quest to understand the role of infections in Alzheimer’s disease is gaining traction. As evidence accumulates, the research community is increasingly convinced of the potential link. However, proving causality and developing effective treatments will require further investigation and collaboration. If pathogens are indeed a contributing factor, addressing this could open new avenues for preventing and treating Alzheimer’s disease.
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