New Study from Oxford Suggests Two Common Vaccines May Lower Dementia Risk

Cognitive decline. Agents such as herpes viruses or pathogen responsible for gingivitis are suspected of promoting the appearance of diseases such as Alzheimer's. The idea that certain chronic or recurring infections could lastingly affect the brain is gaining ground. In this context, vaccination appeared as a promising tool, capable of indirectly preventing this damage by limiting the viral load.

But a study published in 2025 in the journal NPJ Vaccines by a team from the University of Oxford goes further. The researchers observed that two vaccines adjuvanted, Shingrix against the zona and Arexvy against the syncytial respiratory virus, reduced the risk of dementia even beyond their antiviral effect. The protective effect was manifested from the months following the injection, too short a time for a simple prevention of infections alone explains the impact on the brain.

Preventive treatment against dementia is based on already available vaccines

To assess this phenomenon, scientists have analyzed anonymized medical records of more than 130,000 Americans over the age of 60. They compared the effects of different vaccine schemes on the incidence of dementia. As a result, those who received the Shingrix vaccine displayed a reduction of 18% of the risk compared to the vaccinated against flu, while the Arexvy vaccine was associated with a drop of 29%. Even more striking, the combination of the two made it possible to reach a reduction of 37% of the risk within 18 months of vaccination.

This preventive treatment against dementia could therefore be based on targeted stimulation of the immune system. The two vaccines have a particular adjuvant in common, AS01, which seems to trigger beneficial immune responses to the brain. In comparison, classic influenza vaccines, which do not contain this adjuvant, have shown no significant effect on the reduction in the risk of dementia.

Towards an aging medicine redesigned by immune stimulation

The emerging hypothesis is based on a paradigm shift. Rather than seeing dementia as a strictly cerebral process, some researchers are now considering an immune origin within the brain. The AS01 adjuvant, used in Shingrix and Arexvy vaccines, active in particular macrophages and dendritic cells, which could promote a cascade of anti-inflammatory and neuroprotective reactions.

Studies on animal model had already shown that certain components of this adjuvant, such as monophosphoryl lipid A, could reduce the amyloid deposits associated with Alzheimer's disease. The work of the cleat, Todd and Harrison suggest that this immune stimulation could be sufficient, by itself, to trigger a protective effect, without it being necessary to target a specific infection.

This track could open the way to new preventive protocols, no longer centered on the symptomatic treatment of cognitive disorders, but on a fine modulation of the immune system before the appearance of the first clinical signs. An approach that deeply redefines the contours of the prevention of brain aging.