The emerging link between shingles vaccination and reduced Alzheimer’s risk: a public health signal for viral-dementia pathways

Dear Editor, Emerging epidemiological findings suggest that the shingles vaccine, used against the varicella zoster virus (VZV), not only protects against VZV reactivation but also mediates a reduction in the risk of dementia. A recent study has reported that individuals aged over 70 years who received the shingles vaccine named Zostavax demonstrate a reduction in the risk of developing dementia or neurodegeneration by 19.2 percent compared with individuals who had not been vaccinated[1]. Through this study, the authors highlight the first large population-based indications that shingles immunization may confer broader neurological benefits beyond the prevention of herpes zoster. These findings strengthen the hypothesis that shingles vaccination–mediated prevention of VZV reactivation also contributes to the long-term prevention of cognitive impairment. Another piece of evidence comes from a recent study[2]. The study reports a longer period without a dementia diagnosis among individuals vaccinated with the recombinant vaccine Shingrix compared with those vaccinated with the live attenuated zoster vaccine Zostavax, supporting the hypothesis of an association between shingles vaccination and improved neurodegenerative outcomes. Herpes virus remains latent in the neurons for decades and becomes reactivated later in life, mainly due to immune weakness, resulting in inflammatory changes in the neuronal system. This neuroinflammation in the brain causes the activation of microglial cells, leading to pro-inflammatory responses such as the release of cytokines. These inflammatory responses cause degeneration of the neuronal system, contributing to dementia-like symptoms. In chronic infections, neuroinflammation facilitates β-amyloid accumulation, which is a hallmark of Alzheimer’s disease[3]. VZV, being a “neurotropic virus,” affects the neurons and vascular endothelial cells in the CNS. Affected human spinal astrocytes, CSF, and perineural cells show marked deposition of amyloids, β-amyloids, and Aβ peptides[3]. All these pathologies directly contribute to local and systemic inflammation, subsequently leading to neuronal death and dementia. Simultaneously, in people who have suffered from VZV infection, the risk of dementia is threefold higher, with most cases being related to Alzheimer’s disease[3]. Shingles vaccination reduced the dementia risk by limiting viral reactivation, inflammatory stress, and amyloid plaque formation, resulting in decreased neurodegeneration and enhanced protection against dementia by training the immune system[4]. Dementia has been a huge burden on population health worldwide. Even modest reductions in risk at the population level could lead to a substantial decrease in the overall burden of cognitive decline. Vaccination uptake among older adults remains underutilized in many regions, which highlights an important preventive gap[5]. Emerging evidence suggests that expanding adult vaccination programs may lead to better cognitive outcomes. Such approaches may be particularly useful for high-risk groups, such as older adults, immunocompromised individuals, and people with chronic diseases. Collectively, these findings emphasize the need for further mechanistic study to understand the biological pathways underlying this association. If confirmed, the observed relationship may have important public health outcomes, suggesting that vaccination can offer benefits beyond preventing viral infections by contributing to dementia protection.