Overview
Cohort studies suggest an association between long-term exposure to ambient air pollution and the incidence of dementia and cognitive decline, drawing attention to a potentially modifiable cause of dementia, but the biological mechanisms behind are not clear. On one hand, air pollution is known to cause and aggravate cardiovascular health, a major risk factor for dementia. However, other mechanisms, including neuroinflammation and exaggerated protein misfolding could also underlie the association. Air pollution is ubiquitous and unevenly distributed but can be reduced. Understanding the links between pollution and neurodegeneration may impact policies aimed to promote brain equity.
Project Details
Air pollution elevates cytokine expression and oxidative stress in the brain, possibly by continuous activation of microglia. Exposure to air pollution led to increases in Aß42 in mice. Increases in hyperphosphorylated tau and a-synuclein was also observed in small autopsy studies of children and young adults that defined exposure to air pollution by the city of living exclusively. However, it is unclear which of these mechanisms is more relevant or if they have synergic effects.
My hypothesis is that lifetime exposure to air pollution is neurotoxic and plays a role in accelerating neurodegenerative processes of diseases. Through an autopsy approach, I will investigate the correlations of lifetime exposure to urban air pollution with cognitive decline and neurodegenerative changes. I will use an accurate method to assess air pollution exposure at the individual level and a gold-standard definition of neurodegenerative changes (neuropathology), as well as clinical metrics, controlling for possible confounders (e.g. cardiovascular risks, personal habits, and sociodemographic variables).
