We Just Got More Evidence That Two Common Viruses Can Team Up to Trigger Alzheimer's

An experiment on model brains has added more evidence to the hypothesis that there is a link between the two diseases.

While the claim continues to be fiercely debated, researchers at the University of Oxford argue that the presence of two viruses in tandem can promote an excess of Alzheimer's characteristic brain plaques.

Over the years, there has been interest in a possible link between the cold-sore virus and Alzheimer's disease. If you have a gene associated with Alzheimer's, you can have a higher risk of developing the condition if you also have the same genetic abnormality.

The chicken pox virus can linger in nerve cells for a long time and emerge as shingles.

It's possible that the inflammation could increase the risk of dementia, yet shingles rarely erupts more than once or twice in a lifetime. It was thought to be insufficient to cause Alzheimer's.

There are good reasons to think the two conditions are related. Population studies in Taiwan, the UK, South Korea, and the US suggest that vaccine against shingles lowers the risk of dementia.

To get a better idea of what might be going on, the researchers built a brain-like environment within six millimeter wide sponges. These were populated with stem cells that grew into functional neurons and support tissues called glial cells, which kept the neurons alive and well.

There were no signs of an increase in the signature Alzheimer's genes when the brain tissue was only exposed to varicella-zoster.

Exposure to the varicella-zoster virus caused a reactivation of the herpes virus in the neuron.

After this twin-pronged attack, there was a decrease in the signals from the neurons.

The lab studies suggest that if a new exposure to varicella-zoster virus wakes up a dormant herpes simplex virus, they could cause trouble.

There are abnormal clusters of proteins fragments that disrupt nerve signaling in the brain, which can be caused by the presence of alpha-amyloid. Microtubules are usually kept in straight lines with the help of tau. Microtubules start to twist and tangle in people with dementia.

Drugs targeting plaque formation failing to live up to expectations is a matter of ongoing debate. They are a feature of the condition and make it clear that something has gone wrong.

The experiment does not prove that building a brain-like tissue outside the human body is the cause of Alzheimer's disease, according to experts not involved in the study.

They argue that the inflammation is the result of the viral infections, not the specific virus that causes the problem.

"These are laboratory findings and do not directly implicate these viruses as the main cause of Alzheimer's disease, but the results are important and should keep stimulating research," says Paresh Malhotra, a neurologist at Imperial College London.

Future studies will show how viruses play a role in the process of Alzheimer's.

There is a correlation between Alzheimer's disease and the varicella-zoster virus, but what we didn't know is the sequence of events that set the disease in motion.

We believe we have evidence of those events.

The paper was published in a journal.