Scientists have long wondered whether common viral infections might influence the risk of developing Alzheimer’s disease later in life.
Alzheimer’s is the most common form of dementia and slowly destroys memory, thinking, and the ability to carry out everyday activities.
Age remains the biggest risk factor, but researchers now believe that genes, lifestyle, and environmental factors may all contribute to the disease.
A new study from Cardiff University adds another important piece to this puzzle by showing how the body’s immune response to herpesviruses may speed up the development of Alzheimer’s disease.
The study was published in the journal Brain. The researchers focused on herpesviruses, a large family of viruses that includes those responsible for cold sores, infectious mononucleosis, and several common childhood infections.
These viruses are extremely common and often remain in the body for life after the initial infection. Most people never develop dementia, but scientists have suspected for years that these viruses could increase the risk in some individuals.
To investigate this idea, researchers used a well-established mouse model that carries genes associated with Alzheimer’s disease.
They infected the animals with a herpesvirus similar to those that infect humans. Some mice received the antiviral medicine valganciclovir, while others were treated to reduce specific immune cells known as CD4 and CD8 T cells.
The scientists then examined memory, learning ability, brain cell loss, and the buildup of amyloid and tau, two proteins that are closely linked with Alzheimer’s disease. They discovered that infection caused a large number of immune cells to enter the brain. Many of these cells were CD8 T cells that were actively responding to the virus.
The infected mice developed faster cognitive decline than expected. However, mice treated with antiviral medication or treatments that reduced these immune cells performed better on memory tests. This suggests that the immune response triggered by the virus, rather than the virus alone, may contribute to faster disease progression.
The findings also support earlier studies that found similar immune cells in the brains and spinal fluid of people living with Alzheimer’s disease. Although the exact process remains unclear, the study suggests that long-lasting immune activity inside the brain could damage healthy brain tissue over time.
The researchers stress that these findings do not prove that herpesviruses directly cause Alzheimer’s disease. Dementia is a complex condition influenced by many factors, including age, genetics, cardiovascular health, and lifestyle. Instead, the study suggests that viral infections may be one additional factor that increases risk in susceptible people.
The work also highlights the possible value of preventing infections. Vaccination, antiviral medicines, and maintaining a healthy immune system may eventually become part of broader strategies to reduce dementia risk, although much more research is needed before any recommendations can be made.
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Source: Cardiff University.
