A recent study from Brigham and Women’s Hospital in Boston, Massachusetts, has found that individuals who have had shingles, also known as herpes zoster, are at an increased risk of experiencing subjective cognitive decline later in life. Subjective cognitive decline refers to self-perceived cognitive issues that cannot be objectively detected through formal cognitive testing. The study showed a 20% increase in the likelihood of cognitive decline among those who have had shingles, emphasizing the importance of getting vaccinated against this condition.
Shingles is caused by the varicella zoster virus (VZV), the same virus responsible for chickenpox. Once a person has had chickenpox, the VZV virus remains in their body, potentially leading to the development of shingles later in life. The study revealed that individuals who have experienced shingles, especially men carrying the APOE4 gene associated with cognitive impairment and dementia, face a higher risk of subjective cognitive decline compared to women. The link between shingles and cognitive issues highlights the importance of vaccination against shingles, particularly for adults over the age of 50.
Subjective cognitive decline may not always be detected through regular clinical assessments, making it essential for individuals who experience memory or cognitive issues to seek comprehensive neuropsychological testing. While SCD itself may not always progress to more serious cognitive impairments like mild cognitive impairment (MCI) or dementia, studies have shown that individuals with SCD have a higher risk of developing these conditions. Understanding the mechanisms behind cognitive decline and the impact of genetic factors, such as the APOE4 gene, on cognitive health remains an area of ongoing research.
The study’s findings suggest a potential link between the varicella zoster virus and increased risk of vascular diseases, including stroke. Previous data from the cohorts involved in the study showed a 38% higher long-term risk of stroke associated with herpes zoster, persisting for 12 years or longer. This vascular connection may contribute to cognitive decline and increased risk of dementia, as cerebrovascular changes can impact cognitive function. The inflammatory response and neuronal damage triggered by VZV reactivation following post-chickenpox dormancy may play a role in cognitive outcomes, emphasizing the complex interplay between infectious agents, vascular health, and brain function as individuals age.
Vaccination against shingles is highlighted as a crucial step in reducing the risk of cognitive decline associated with herpes zoster. Research has shown that higher rates of shingles vaccination are linked to lower rates of dementia, reinforcing the importance of preventive measures in safeguarding cognitive health. Further studies are needed to explore the sex-specific effects observed in individuals with the APOE4 gene and the impact of genetic, hormonal, and Alzheimer’s pathology factors on cognitive outcomes. Understanding these complexities can provide valuable insights into the role of infectious agents, vascular health, and genetic predispositions in cognitive decline and dementia risk among aging populations.
