See professor Shawn Gale's website here.
Research Interests
The global dementia epidemic continues to grow, with projected cases expected to more than double by 2050. Despite intensive effort, disease-modifying therapies remain elusive, underscoring the urgent need to identify potentially modifiable risk factors that can delay or prevent dementia onset. In our lab, we investigate two broad yet underrecognized domains of risk: infectious disease burden and environmental exposures, which interact with immune, vascular, and neuroinflammatory pathways to influence cognitive function, and may hasten cognitive decline, dementia, and neuropsychiatric vulnerability.
Our recent work demonstrates that common infections, including Helicobacter pylori, cytomegalovirus, herpesviruses, Toxoplasma gondii, and periodontal pathogens, are associated with measurable cognitive impairment in otherwise healthy adults, suggesting that subclinical infection effects precede dementia onset. These same exposures are also linked to heightened risk for psychiatric disorders such as depression, anxiety, and psychosis, pointing to shared mechanistic pathways that cross diagnostic boundaries. Complementary research on environmental pollutants shows that long-term exposure to fine particulate matter and nitrogen oxides is associated with hippocampal and frontal cortical atrophy, white matter changes, and increased risk of dementia, stroke, and psychiatric illness. Together, these findings position infection and air pollution as convergent, potentially modifiable drivers of brain health outcomes.