Chronic Gut Virus May Play a Role in Alzheimer’s Development

Summary: Experts have linked serious intestinal diseases caused by cytomegalovirus ( HCMV) to a unique type of Alzheimer’s disease. The vagus nerve may be where the virus travels from the intestines to the head, altering immune reactions and causing amyloid plaque and tau tangles, which are mark Alzheimer’s conditions.

Although HCMV infection is common and generally unaffected, this research discovered that some people may develop severe brain inflammation as a result. The experts demonstrated how HCMV causes chemical changes in human brain cell designs that are related to Alzheimer’s.

These studies highlight the potential for antimicrobial treatments to treat this type of Alzheimer’s. The focus of ongoing work is to create a blood test to identify individuals who have a serious HCMV infection and examine treatment options.

Important Facts:

    Gut-to-Brain Link: HCMV infection in the gut does reach the brain via the ventral brain, contributing to Alzheimer’s.

  • Chemical Impact: The malware triggers amyloid and beta production, leading to nerve damage.
  • Medical Potential: Scientists are exploring antimicrobial drugs to treat this Alzheimer’s type.

Origin: Arizona State University

Arizona State University and Banner Alzheimer’s Institute experts, along with their partners, have discovered a shocking connection between a continual gut disease caused by a typical virus&nbsp, and the development of Alzheimer’s illness in a subset of people.

Most people are thought to be exposed to this disease, known as herpes or HCMV, during the first few years of existence. Although it is not regarded as a sexually transmitted disease, the herpes virus herpes is one of nine. The virus typically spreads through bodily fluid publicity, but it does not when it is effective.

The malware then travels to the head through the vagus nerve or into the bloodstream. Credit: Neuroscience News

In some individuals, the disease may remain active in the colon, where it may pass through the vagus nerve, a crucial information link between the gut and the head, according to the new research. Once there, the virus may modify the immune system and lead to additional changes associated with Alzheimer’s disease.

If the scientists ‘ theories are confirmed, they might be able to determine whether current antiviral treatments can handle or stop this type of Alzheimer’s disease. A blood test is being developed to identify those who are already suffering from an energetic HCMV infection and who may benefit from antiviral therapy.

” We think we found a biologically unique type of Alzheimer’s that may affect 25 % to 45 % of people with this disease”, said Dr. &nbsp, Ben Readhead, co-first author of the study and research associate professor with ASU-Banner Neurodegenerative Disease Research Center in the Biodesign Institute at ASU.

This type of Alzheimer’s has the hallmark amyloid plaques and tau tangles, which are microscopic brain abnormalities used to diagnose dementia, and has a specific genetic profile of the brain’s virus, antibodies, and defense cells.

The findings were published today in” Alzheimer’s &amp, Dementia: The Journal of the Alzheimer’s Association”.

Researchers from ASU, Banner Alzheimer’s Institute, Banner Sun Health Research Institute, and the Translational Genomics Research Institute ( TGen ) led the collaborative effort, which included investigators with UMass Chan Medical School, Institute for Systems Biology, Rush University Medical Center, Icahn School of Medicine at Mount Sinai, and other institutions.

The research group believes that some people who are exposed to HCMV produce severe intestinal infections. The virus finally enters or travels through the vagus nerve to the head through the vagus nerve.

That, it is recognized by the body’s immune cells, called microglia, which turn on the appearance of a certain protein called CD83. The disease may be a factor in the natural modifications that lead to Alzheimer’s disease. &nbsp,

The position of the body’s immune cells

Microglia, or the body’s immune cells, are activated when responding to infection. Although originally safe, a persistent increase in microglial exercise may cause chronic swelling and neuronal damage, which are both factors in the development of neurological conditions, including Alzheimer’s.

In a study published earlier this year in” Nature Communications“, the researchers found that the postmortem brains of research participants with Alzheimer’s disease were more likely than those without Alzheimer’s to harbor specifically CD83 ( + ) microglia.

They discovered an antibody in the bowels of these subjects as they investigated why this happened, which raises the possibility that an infection might be causing this type of Alzheimer’s.

Researchers in the most recent study sought to understand what might be influencing the production of intestinal antibodies. The team discovered that the antibodies were precisely anti-HCMV when they were examined in the spinal fluid of these same individuals. This led to a search for proof of HCMV infection in these subjects ‘ intestines and head cells, which they discovered.

They also observed HCMV in the same content ‘ ventral nerves, which raises the possibility that this is how the virus enters the brain. Working with RUSH University, the researchers were able to reproduce the association between cytomegalovirus infection and CD83 ( + ) microglia in an independent cohort of Alzheimer’s patients.

The analysis team used animal head battery models to further investigate the impact of this virus and show its ability to cause chemical changes related to this particular type of Alzheimer’s disease. The virus ‘ contact did lead to an increase in the production of amyloid and activated tau proteins, which contributed to the degradation and death of cells.

Is HCMV to blame for Alzheimer’s disease in some folks?

HCMV is able to harm people of all ages. In most healthy individuals, disease occurs without signs but may manifest as a gentle, flu-like disease. By the age of 80, about 80 % of people have antibodies.

However, the researchers merely found bowel HCMV in a select few people, and this disease appears to be a contributing factor in the presence of the disease in the brain. For this reason, the analysts note that just coming into contact with HCMV, which happens to almost everyone, should not be cause for concern.

No second pathogen has consistently been linked to Alzheimer’s disease, despite researchers ‘ proposals more than 100 years ago that dangerous viruses or bacteria may contribute to the condition.

These two studies, according to the researchers, demonstrate the potential effects that infections can have on brain health and neurodegeneration in general. They continue, adding that independent studies are required to evaluate both their findings and the hypotheses that led to them.

The NOMIS Foundation, Banner Alzheimer’s Foundation, National Institutes of Health, and Arizona Alzheimer’s Consortium supported the study. Arizona’s unique biorepositories, particularly the Brain and Body Donation Program at Banner Sun Health Research Institute, provided tissue samples and resources, including the colon, vagus nerve, brain and spinal fluid.

Additional brain samples and data were provided by Rush University’s Religious Orders Study and Memory and Aging Study. This allowed researchers to conduct a more nuanced investigation, highlighting the systemic rather than purely neurological roots of Alzheimer’s disease.

” Having access to different tissues from the same people was extremely important to us.” That made it possible to combine the findings. We’re grateful to the Banner Health Brain and Body Donation Program for its assistance, said Readhead, who is also the Edson Endowed Professor of Dementia Research at the center. Arizona is the only place I know of where a study like this could have been conducted.

” We are extremely grateful to our research participants, colleagues, and supporters for the chance to advance this research in a way that none of us could have done on our own”, said Dr. Eric Reiman, Executive Director of Banner Alzheimer’s Institute and the study’s senior author.

” We’re excited about the chance to have researchers test our findings in ways that make a difference in the study, subtyping, treatment and prevention of Alzheimer’s disease” .&nbsp,

Could antiviral medications help treat Alzheimer’s patients who have a chronic HCMV infection, according to the recent study’s findings?

The investigators are currently developing a blood test to identify individuals who have this particular chronic intestinal HCMV infection. They want to see whether existing antiviral medications can be used to treat or prevent this type of Alzheimer’s disease in conjunction with new Alzheimer’s blood tests to see if they can use them.

Research institutions involved in the study, published in the journal Alzheimer’s &amp, Dementia: ASU-Banner Neurodegenerative Disease Research Center in the Biodesign Institute at ASU, Weill Cornell Medicine, Icahn School of Medicine, University of Massachusetts Chan Medical School, The Translational Genomics Research Institute, Institute for Systems Biology, Serimmune, Inc, Rush University Medical Center, Banner Sun Health Research Institute, and Banner Alzheimer’s Institute.

About this microbiome and Alzheimer’s disease research news

Author: Sandy Keaton Leander
Source: Arizona State University
Contact: Sandy Keaton Leander – Arizona State University
Image: The image is credited to Neuroscience News

Original Research: Open access.
” Alzheimer’s disease-associated CD83 ( + ) microglia are linked with increased immunoglobulin G4 and human cytomegalovirus in the gut, vagal nerve, and brain” by Ben Readhead et al. Alzheimer’s &amp, Dementia


Abstract

Alzheimer’s disease-associated CD83 ( + ) microglia are linked with increased immunoglobulin G4 and human cytomegalovirus in the gut, vagal nerve, and brain

INTRODUCTION

While there may be microbial contributions to Alzheimer’s disease ( AD), findings have been inconclusive. We recently discovered a CD83 ( + ) microglia subtype with AD that had an increased immunoglobulin G4 ( IgG4 ) in the transverse colon (TC ).

METHODS

We used immunohistochemistry ( IHC), IgG4 repertoire profiling, and brain organoid experiments to explore this association.

RESULTS

CD83 ( + ) microglia in the superior frontal gyrus ( SFG ) are associated with elevated IgG4 and human cytomegalovirus ( HCMV) in the TC, anti-HCMV IgG4 in cerebrospinal fluid, and both HCMV and IgG4 in the SFG and vagal nerve. This relationship was repeated in a blind AD cohort. HCMV-infected cerebral organoids showed accelerated AD pathophysiological features ( Aβ42 and pTau-212 ) and neuronal death.

DISCUSSION

Findings point to complex, cross-tissue interactions between CD83 ( + ) microglia and the adaptive immune response associated with HCMV in AD patients. This may indicate an opportunity for antiviral therapy in persons with AD and biomarker evidence of HCMV, IgG4, or CD83 ( + ) microglia.

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