A new study from Brigham and Women’s Hospital in Boston, MA, has found that individuals who have had shingles are at a higher risk of developing subjective cognitive decline (SCD), which could potentially lead to more serious cognitive issues. Shingles is caused by the varicella zoster virus (VZV), the same virus responsible for chickenpox. After the chickenpox infection resolves, the virus remains in the body, and individuals who have had chickenpox are at risk of developing shingles unless they are vaccinated. The study highlights the importance of being vaccinated against shingles to lower the risk of cognitive decline later in life.
Men who carry a certain gene, APOE4, are at a somewhat higher risk of cognitive issues compared to women. Additionally, the study found that individuals who have had shingles may be more likely to experience subjective cognitive decline if they carry the APOE4 gene. Subjective cognitive decline is a state where self-perceived cognitive decline is present, but objective cognitive impairments cannot be detected through formal testing. While subjective cognitive decline may be mild, there is concern that it could progress to more serious cognitive issues in the future.
The study also revealed a higher risk of subjective cognitive decline for men with the APOE4 gene who have had shingles compared to women. The reasons behind this sex-specific difference remain unclear, but previous research has shown sex differences in how genetic risk factors relate to Alzheimer’s disease and neurodegeneration. Further research is needed to better understand the mechanisms behind these sex-specific effects and the higher incidence of subjective cognitive decline among men with the APOE4 gene.
Researchers have suggested a possible link between the varicella zoster virus (VZV) and an increased risk of vascular diseases, including stroke. Data from the study’s cohorts showed that individuals who had herpes zoster, or shingles, had up to a 38% higher long-term risk of stroke, persisting for 12 years or longer. This vascular connection may play a role in cognitive decline and dementia risk, as changes in cerebrovascular health can contribute to cognitive impairment. Inflammation and direct neuronal damage from VZV reactivation after post-chickenpox dormancy may also be factors in cognitive outcomes.
In conclusion, the study provides valuable insights into the potential link between shingles, subjective cognitive decline, and cognitive impairment later in life. It underscores the importance of being vaccinated against shingles to lower the risk of developing cognitive issues. Further research is needed to explore the sex-specific effects of the APOE4 gene on subjective cognitive decline and to better understand the mechanisms behind these effects. The study highlights the complex interplay between infectious agents, vascular health, and brain function as we age and emphasizes the importance of preventive measures such as vaccination to protect cognitive health.
