Scientists discover common virus may cause type of Alzheimer’s disease

Researchers have discovered a link between a chronic intestinal infection caused by a common virus and the development of Alzheimer’s disease in some people.

Most people are exposed to cytomegalovirus (CMV) during childhood, and after initial infection, the virus remains in the body for its entire life, usually dormant.

By the age of 80, 9 out of 10 people will have antibodies indicative of CMV in their blood. A type of herpesvirus, the pathogen spreads via bodily fluids (such as breast milk, saliva, blood, and semen), but only when the virus is active.

In one unlucky group, the study showed, the virus may have found a biological loophole where it can stay active long enough to travel up the gut-brain highway, known more formally as the vagus nerve.

Upon reaching the brain, the active virus has the potential to worsen the immune system and contribute to the development of Alzheimer’s disease.

That’s a worrying possibility, but it also means that antiviral drugs could prevent some people from developing Alzheimer’s disease, especially if researchers can develop blood tests to quickly detect active CMV infection in the gut.

Earlier this year, some members of the Arizona State University team announced a link between a subtype of microglia associated with Alzheimer’s disease, named CD83(+) because of the cell’s genetic quirks, and elevated levels of immunoglobulin G4 in the transverse colon, which hints at some sort of infection.

Microglia are the cells responsible for cleaning throughout the central nervous system. They scavenge for plaques, debris, and excess or broken neurons and synapses, eating away at them when possible and sounding alarms when infection or damage is out of control.

They’re there to help, but if microglia are constantly triggered, releasing their inflammatory weapons without pause, it can lead to the neuronal damage associated with Alzheimer’s disease.

“We believe we have discovered a biologically unique subtype of Alzheimer’s disease that may affect 25 to 45 percent of people with this disease,” said biomedical scientist and lead author Ben Readhead of Arizona State University.

“This subtype of Alzheimer’s disease includes the characteristic amyloid plaques and tau tangles – microscopic brain abnormalities used for diagnosis – and has a distinct biological profile of viruses, antibodies and immune cells in the brain .”

The researchers had access to a range of organ tissues, including colon, vagus nerve, brain and cerebrospinal fluid, from 101 donors, 66 of whom had Alzheimer’s disease. This helped them study how the body’s systems interact with Alzheimer’s disease, often viewed from a purely neurological perspective.

They traced the presence of anti-CMV antibodies from the donors’ intestines, to their spinal fluid, to their brains, and even discovered the virus itself hidden in the donors’ vagus nerves.

The same trends emerged when they repeated the study in a separate, independent cohort.

Human brain cell models provided further evidence of the virus’s involvement, increasing the production of amyloid proteins and phosphorylated tau proteins and contributing to neuron degeneration and death.

It is important to note that these links were only found in a very small subset of individuals with chronic intestinal CMV infection. Since almost everyone comes into contact with CMV, simply being exposed to the virus is not always a cause for concern.

Readhead and his team are working to develop a blood test that will detect CMV intestinal infection so it can be treated with antiviral drugs and perhaps prevent patients from developing this type of Alzheimer’s disease.

The research was published in Alzheimer’s and dementia: the journal of the Alzheimer’s association.

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