Cold sore link to Alzheimer’s not proven

People who suffer from cold sores are more likely to develop Alzheimer’s disease, newspapers reported today.

The Daily Telegraph said that a study has found that exposing brain cells to the herpes simplex virus (HSV-1) that causes cold sores, results in large quantities of a protein to build up in the brain - a state that is commonly found in Alzheimer’s sufferers. This effect is especially apparent in people who have a type of gene variant that is “carried by 30% of the population and half of all Alzheimer’s patients”.

New Scientist said that “80% of elderly people carry HSV-1, so any exacerbating effect could be having a huge impact.”

The BBC reported that “Scientists believe the discovery could pave the way for a vaccine that may help prevent the brain disorder.”

The news reports are based on laboratory research where scientists infected human and animal brain cells with HSV-1 to see how it affects the build up of the amyloid protein that forms plaques in the brains of those with Alzheimer’s disease.

This study does not provide enough reliable evidence to confirm a link between the two conditions and extensive further research is needed before any firm conclusions can be drawn. A vaccine for HSV-1 is also a long way off.

Alzheimer’s disease and its possible causes are still poorly understood. At this stage people with the extremely common, recurrent infection of cold sores, should not think that they are at an increased risk of developing Alzheimer’s.

Where did the story come from?

This research was carried out by Matthew Wozniak and colleagues of the University of Manchester. Support grants were received from the Fidelity Foundation and Henry Smith Charity. The study was published in the peer-reviewed scientific journal: Neuroscience Letters.

What kind of scientific study was this?

This was a laboratory study using human and animal brain cells to see whether infection with HSV-1 increases the build up of the amyloid protein that is seen in the brains of people with Alzheimer’s disease.

The researchers used two special types of brain cancer cell that can be grown in the laboratory. Some of these cells were infected with HSV-1 while some were left uninfected. A technique that makes the proteins show up as staining in the cells when examined under the microscope, was then used to look for the two common forms of amyloid protein in the cells.

The researchers also looked for the precursor form of amyloid and HSV-1 to confirm that it was present within the brain cells.

They also infected some mice with the HSV-1 virus and left some uninfected, and then again looked for these amyloid proteins in the mice’s brains. They also conducted other experiments on the human cells and on monkey kidney cells to look at how HSV-1 might affect amyloid protein levels.

What were the results of the study?

The researchers found that the cells that were infected with HSV-1 had increased quantities of both types of amyloid protein, and decreased levels of the precursor protein. They found that mice infected with HSV-1 had a build up of one form of the amyloid protein in their brains, but uninfected mice did not.

What interpretations did the researchers draw from these results?

The researchers conclude that infection of brain cells with HSV-1 increases the amount of amyloid protein present. They say that their findings “show that HSV-1 can directly contribute to the development of senile plaques” and that the findings “further support our contention that treatment of Alzheimer’s dementia patients with antiviral agents would reduce, or even prevent further cognitive decline”.

What does the NHS Knowledge Service make of this study?

While these studies indicate an avenue for further research, at present they do not provide convincing evidence of a link between Alzheimer’s and the HSV-1 virus.

These were studies under experimental conditions where samples of brain cells were exposed to high levels of the virus, and as such cannot be considered a direct parallel to the situation where infection occurs in the living human body. The researchers do not report how many times they repeated their experiments to confirm their results, but numbers are likely to be small, and would need independent confirmation by other researchers.

Interpreting the findings also relies upon the assessor’s subjective assessment of the degree of protein staining that was present, which may lead to some inaccuracies.

Sir Muir Gray adds...

An interesting theory and possibility, but there are still many steps to take to test the theory. In the meantime a cold sore is a cold sore - and no more.