Do Viruses Cause Alzheimer’s?

According to an American-British study, the pathogens that cause chickenpox and shingles together can trigger dementia.

Research in this important area was rocked just a few weeks ago by a scientific scandal involving apparently inaccurate studies on the development of Alzheimer’s. It is still only partially understood which processes lead to changes in the brain; What sets them in motion remains a mystery. Researchers from Tufts University in Massachusetts (USA) and the University of Oxford (England) have now added one piece – or more – of the puzzle to answer this question. The US-British team reinforces the suspicion that varicella zoster and herpes simplex virus play a role – and have decoded a mechanism by which the two pathogens cause damage in the brain.

According to the study, the varicella-zoster virus (VZV), which causes chickenpox and shingles, can activate the herpes simplex virus “to initiate the early stages of Alzheimer’s disease,” according to a statement from Tufts University. The findings were published in the journal “Journal of Alzheimer’s Disease.”

Herpes simplex and varicella zoster virus are among the most common viruses of all. Both belong to the herpes virus family, after a severe illness both remain in the body as “sleepers” and can be reactivated; Symptoms that may be important for the development of Alzheimer’s. It is estimated that 95 percent of people contract varicella zoster before the age of 20. In most cases, this leads to chickenpox, and subsequent reactivation of the virus for painful shingles (herpes zoster).

According to the World Health Organization, about 3.7 billion people under the age of 50 are infected with HSV-1, one of the most common forms of herpes simplex. HSV-1 causes uncomfortable blisters on the lips. It spends most of its time silently in the body without any symptoms, lying dormant in nerve cells; Even in the brain. In the active state, however, the HSV-1 virus can accumulate amyloid beta and tau proteins there, according to a Tufts University statement.

Both proteins undergo malignant transformation in Alzheimer’s. For example, fragments of amyloid beta protein can clump together to form plaques, and tau proteins can form twisted, elongated filaments called filaments. However, how these processes are connected and exactly what they do is not yet fully understood. The supposedly false studies also revolved around this complex of questions.

An American-British research team now claims to have discovered that varicella-zoster virus infection triggers inflammatory processes, which in turn awaken the dormant herpes simplex virus in the brain. The possibility of a connection between the herpes simplex virus and Alzheimer’s has been discussed for some time. One of the first to raise this doubt and research it is neuroscientist Ruth Itzhaki from the University of Cambridge and the University of Oxford. She was also involved in the current study.

“We know that there is an association between HSV-1 and Alzheimer’s disease, and some have suggested that VZV may also be involved. But what we didn’t know is the sequence of events that causes the virus to initiate the disease. to produce,” says David Kaplan, head of the Department of Biomedical Engineering at Tufts School of Engineering. “We think we now have evidence of these events.”

For their study, the researchers used a three-dimensional human tissue culture model that mimics the brain. They reproduced its structures in tiny, six-millimeter-wide sponges made of silk protein and collagen. They in turn populate the sponge with neural stem cells, which become functional neurons capable of transmitting signals in a network – as in the real brain.

Researchers found that neurons cultured in brain tissue can become infected with varicella zoster. However, this alone did not lead to the formation of the proteins amyloid beta and tau, which are central to Alzheimer’s. However, if neurons harbored an inactivated herpes simplex virus-1, exposure to varicella zoster resulted in its reactivation – leading to a “dramatic increase” in tau and amyloid beta proteins. The result: neuronal signals slowed down.

Dana Cairns of Tufts University explains, “It’s a double whammy of two viruses that are common and usually harmless, but laboratory studies suggest they can cause problems when new exposure to VZV has inactivated HSV-1.” goes.”

The researchers also observed that samples infected with Varicella zoster began to produce cytokines. Cytokines are proteins that are involved in inflammatory processes – and in fact, inflammation caused by infection can be seen in brain tissue. Presumably, according to David Kaplan, this inflammation caused the dormant herpes simplex virus to become active in the brain—and lead to even more inflammation. Researchers have mainly looked at the risk of Alzheimer’s from repeated activation of herpes simplex in the brain. Vaccination against chickenpox can “reduce it significantly”.

However, it is also “still possible that other infections and other pathways can lead to Alzheimer’s disease,” says Dana Cairns. Interactions with risk factors such as head trauma, severe obesity and alcohol consumption are also conceivable. The coronavirus was also suspected to be able to trigger Alzheimer’s, but a causal relationship could not be proven. A large Danish study found that the risk of Alzheimer’s and Parkinson’s increases from six months to a year after infection, but the same applies to influenza and bacterial pneumonia. So some scientists suspected that the cause was less the coronavirus itself and more inflammation associated with the infection.

An American-British research team is now bringing into play that Sars-CoV-2 can reactivate both dormant varicella zoster and herpes simplex virus in the body. It is wise to keep this in mind, they write.