Cold sores are usually seen as a minor annoyance, but could viruses related to cold sores have effects that last for decades?
According to new research from Cardiff University, the answer may be more complicated than scientists once believed.
The study suggests that the body’s own immune response to herpesviruses may help speed up the changes seen in Alzheimer’s disease, offering a new direction for dementia research.
Alzheimer’s disease affects millions of people worldwide and is the leading cause of dementia. It gradually damages memory, thinking, language, and independence. Although scientists have identified abnormal proteins such as amyloid and tau as key features of the disease, they still do not fully understand what starts the damaging process.
Previous studies hinted that common infections might be involved, especially herpesviruses, which remain dormant inside the body after infection. These viruses include those that cause cold sores and glandular fever.
The new study, published in Brain, explored how the immune system reacts to these viruses and whether that response affects the brain.
Researchers used genetically modified mice that naturally develop changes similar to Alzheimer’s disease. After infecting the mice with a herpesvirus, they carefully monitored memory, learning, brain cell health, and the accumulation of amyloid and tau proteins. They also tested whether antiviral treatment or reducing certain immune cells could change the outcome.
The results showed that infection attracted large numbers of T cells into the brain. These immune cells are normally essential for fighting viruses, but in this case they appeared to be associated with faster memory decline. When the mice received antiviral medicine or treatments that reduced these virus-fighting T cells, their cognitive performance improved compared with untreated animals.
The study suggests that an overactive or prolonged immune response may unintentionally contribute to damage in the brain. Researchers also noted that similar virus-targeting T cells have previously been found in people with Alzheimer’s disease, making the findings even more interesting.
Despite these promising results, the scientists caution against jumping to conclusions. The study does not show that herpesviruses are the direct cause of Alzheimer’s disease, and many people infected with these common viruses never develop dementia. Alzheimer’s remains a complicated disease influenced by genetics, aging, cardiovascular health, lifestyle, and possibly infections working together.
The research does, however, point to exciting possibilities for the future.
Better infection prevention, vaccines, antiviral drugs, and treatments that carefully control harmful immune responses could eventually become part of strategies aimed at reducing dementia risk. Scientists now need clinical studies to determine whether the same biological process occurs in people.
If you care about Alzheimer’s, please read studies about Vitamin D deficiency linked to Alzheimer’s, vascular dementia, and Oral cannabis extract may help reduce Alzheimer’s symptoms.
For more health information, please see recent studies about Vitamin B9 deficiency linked to higher dementia risk, and results showing flavonoid-rich foods could improve survival in Parkinson’s disease.
Source: Cardiff University.
