A fascinating link has emerged from recent scientific investigations, connecting a long-lasting gut infection caused by the common cytomegalovirus (HCMV) to Alzheimer’s disease onset in a particular group of individuals.
This herpes virus, which many people encounter in their early years, has provided new insights thanks to groundbreaking research conducted by teams from Arizona State University and the Banner Alzheimer’s Institute, along with other esteemed collaborators.
Mechanisms Linking HCMV to Alzheimer’s Disease
Current evidence indicates that HCMV may persist in the gut, establishing pathways to the brain through the vagus nerve—a key channel between our gut and brain.
When the virus makes its way into the brain, it can disrupt immune responses and trigger brain changes that are known to characterize Alzheimer’s disease.
Thus, HCMV stands out as a potential target for antiviral treatments.
While HCMV is one of nine herpes viruses, it’s crucial to note that it isn’t classified as a sexually transmitted infection.
The virus spreads through infected bodily fluids and tends to reactivate under specific conditions.
Research Findings and Implications
The research team hypothesizes that a significant percentage of Alzheimer’s patients—between 25% and 45%—may have a distinct biological subtype of the disease.
This variant not only shows the hallmark amyloid plaques and tau tangles associated with Alzheimer’s but also exhibits a unique signature of viral presence, immune activity, and antibodies in the brain.
This informative study, published in “Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association,” is the result of collaborative efforts among experts from ASU, Banner Alzheimer’s Institute, UMass Chan Medical School, and Mount Sinai’s Icahn School of Medicine.
The findings suggest that after exposure to HCMV, a chronic intestinal infection could develop, providing the virus an entry point into the bloodstream or allowing it to traverse the vagus nerve straight to the brain.
Once there, it can activate microglia, the brain’s immune cells, prompting them to express a gene called CD83.
This activation may contribute to the biological shifts linked with Alzheimer’s.
The Future of Alzheimer’s Research and Treatment
Initially, microglia serve as protectors of the brain in response to infections, but continuous activation can lead to persistent inflammation and neuronal harm—both of which are associated with the progression of neurodegenerative diseases like Alzheimer’s.
Prior research highlighted in “Nature Communications” revealed that postmortem brain evaluations showed an increased presence of CD83(+) microglia in individuals with Alzheimer’s compared to those without the disease.
This discovery led scientists to investigate the presence of antibodies related to HCMV in the intestines of these individuals.
The current research dives deeper, examining spinal fluid samples to confirm that antibodies specifically targeted HCMV.
It also explored the presence of the virus in both intestinal and brain tissues, thus reinforcing the association.
Moreover, researchers identified HCMV along the vagus nerve in the same study group, hinting at this as a route through which the virus might access the brain.
In collaboration with RUSH University, their findings linked HCMV infection to the prevalence of CD83(+) microglia in another cohort of Alzheimer’s patients.
To investigate the implications of HCMV, scientists utilized human brain cell models, where they observed that the virus triggered molecular changes characteristic of this specific Alzheimer’s variant.
Notably, HCMV exposure led to increased production of amyloid and phosphorylated tau proteins, intensifying neuronal degeneration and promoting cell death.
While HCMV can infect individuals at any age—often without symptoms—the study found its intestinal form present only in a subset of participants.
Researchers clarify that widespread exposure to HCMV is not a cause for worry, as it does not necessarily signify a risk for Alzheimer’s disease.
Despite decades of speculation regarding the influence of microbes on Alzheimer’s, no singular pathogen had been conclusively linked to the condition until this research.
These findings suggest broader implications concerning infections and their impact on brain health and neurodegenerative disease progression.
The research team, however, underscores the necessity for more independent studies to validate their findings.
Support for this study came from organizations like the NOMIS Foundation, the Banner Alzheimer’s Foundation, the National Institutes of Health, and the Arizona Alzheimer’s Consortium.
The researchers benefitted significantly from unique tissue samples provided by the Brain and Body Donation Program at the Banner Sun Health Research Institute, which allowed them to conduct an in-depth analysis of the interconnected physiological systems at play in Alzheimer’s disease.
The collaborative nature of the research in Arizona sets a model for future studies in the field.
It raises an intriguing question: could antiviral treatments prove beneficial for Alzheimer’s patients suffering from chronic HCMV infections? The research team is currently developing a blood test to identify those with such infections.
They aim to combine this tool with emerging blood tests for Alzheimer’s, paving the way for evaluating the therapeutic potential of existing antiviral drugs to manage or perhaps prevent this specific Alzheimer’s variant.
Source: ScienceDaily