PM2.5 exposure in association with AD-related neuropathology and cognitive outcomes

Particulate matter with a diameter of less than 2.5 mu m or PM2.5 is recognized worldwide as a cause of public health problems, mainly associated with respiratory and cardiovascular diseases. There is accumulating evidence to show that exposure to PM2.5 has a crucial causative role in various neurological disorders, the main ones being dementia and Alzheimer's disease (AD). PM2.5 can activate glial and microglial activity, resulting in neuroinflammation, increased intracellular ROS production, and ultimately neuronal apoptosis. PM2.5 also causes the alteration of neuronal morphology and synaptic changes and increases AD biomarkers, including amyloid-beta and hyperphosphorylated-tau, as well as raising the levels of enzymes involved in the amyloido-genic pathway. Clinical trials have highlighted the correlation between exposure to PM2.5, dementia, and AD diagnosis. This correlation is also displayed by concordant evidence from animal models, as indicated by increased AD biomarkers in cerebrospinal fluid and markers of vascular injury. Blood-brain barrier disruption is another aggravated phenomenon demonstrated in people at risk who are exposed to PM2.5. This review sum-marizes and discusses studies from in vitro, in vivo, and clinical studies on causative relationships of PM2.5 exposure to AD-related neuropathology. Conflicting data are also examined in order to determine the actual association between ambient air pollution and neurodegenerative diseases.

Automated summary

PM2.5 is recognized worldwide as a cause of public health problems, particularly associated with respiratory and cardiovascular diseases. Exposure to PM2.5 is increasingly linked to neurological disorders, such as dementia and Alzheimer's disease, through mechanisms including neuroinflammation, increased ROS production, and neuronal apoptosis.