Vaccines appear to have a meaningful impact on the progression and risk of Alzheimer’s disease and related dementias, though the relationship is complex and still under active investigation. Several lines of evidence suggest that certain vaccines, especially those targeting infections like shingles, respiratory syncytial virus (RSV), influenza, and pneumonia, may reduce the risk of developing dementia or slow its progression.
One key insight is that infections themselves can increase the risk of dementia. When the brain or body is exposed to infections, inflammatory processes may accelerate neurodegeneration or worsen Alzheimer’s pathology. Vaccines that prevent these infections could therefore indirectly protect the brain by reducing inflammation and infection-related damage. For example, studies have shown that people vaccinated against shingles or RSV had a significantly lower risk of being diagnosed with dementia compared to those who only received flu vaccines. The combined vaccination against both shingles and RSV showed an even stronger protective effect, suggesting a cumulative benefit from preventing multiple infections.
Beyond infection prevention, some vaccines may influence Alzheimer’s disease through specific immune system pathways. Certain vaccine components, such as the AS01 adjuvant system used in shingles vaccines, stimulate immune receptors like toll-like receptor 4. This stimulation might modulate immune responses in a way that reduces Alzheimer’s pathology, as seen in animal models where components like monophosphoryl lipid A improved Alzheimer’s-related brain changes. This points to a possible direct immunological mechanism by which vaccines could slow or alter disease progression, independent of infection prevention.
In addition to vaccines for infectious diseases, there is ongoing research into vaccines designed specifically to target Alzheimer’s disease itself. These experimental vaccines aim to clear or prevent the buildup of toxic proteins in the brain, such as amyloid-beta plaques and tau neurofibrillary tangles, which are hallmarks of Alzheimer’s. For instance, a vaccine candidate called ALZ-101 is in clinical trials to stimulate the immune system to attack amyloid-beta oligomers, potentially slowing disease progression. Another approach involves vaccinating against modified tau protein fragments to reduce tau aggregation, which could delay neurodegeneration with minimal side effects. These Alzheimer’s-specific vaccines represent a promising frontier but are still in early stages of development.
Vaccination also appears to reduce mortality and complications in people who already have dementia. Since infections can be particularly dangerous for individuals with cognitive decline, vaccines against flu and pneumonia help lower the risk of severe illness and death in this vulnerable population. This protective effect may indirectly contribute t
