First Advisor
Jon Fink
Date of Award
Spring 6-12-2026
Document Type
Thesis
Degree Name
Bachelor of Science (B.S.) in Science and University Honors
Language
English
Subjects
wildfire-derived PM2.5, neuroinflammation, Alzheimer’s disease, Parkinson’s disease, neurodegenerative disease progression, environmental health policy
Abstract
Neurodegenerative diseases represent a growing global health burden, yet many remain poorly understood and lack effective curative or preventive interventions. As the prevalence of Alzheimer’s disease and Parkinson’s disease continues to rise, increasing attention has been placed on modifiable environmental exposures that may contribute to disease progression. Wildfire-derived fine particulate matter (PM2.5) has emerged as an increasingly important air-quality concern in the United States, eroding prior gains in ambient pollution reduction and creating recurrent episodes of unhealthy air exposure. This narrative review synthesizes current evidence linking wildfire-derived and ambient PM2.5 exposure to neuroinflammatory pathways relevant to neurodegenerative disease progression. PM2.5 may affect the central nervous system through multiple overlapping routes, including pulmonary deposition with systemic inflammatory signaling, direct olfactory transport, blood-brain barrier disruption, gut barrier dysfunction, microglial priming, mitochondrial injury, oxidative stress, and persistent epigenetic or RNA-mediated alterations. These generalized mechanisms may intersect with disease-specific vulnerabilities in Parkinson’s disease and Alzheimer’s disease. In Parkinson’s disease, PM2.5-induced inflammation and oxidative stress may amplify dopaminergic neuron vulnerability and α-synuclein–associated feed-forward inflammatory loops. In Alzheimer’s disease, these same mechanisms may promote amyloidogenic processing, tau hyperphosphorylation, synaptic injury, and impaired protein clearance. This review also considers the public-health implications of wildfire smoke within current air-quality policy, particularly the disconnect between regulatory exclusion of exceptional wildfire events and continued biological exposure among affected populations. While causality remains incompletely established, the convergence of epidemiological, toxicological, and mechanistic evidence supports further investigation of wildfire-derived PM2.5 as a plausible environmental amplifier of neurodegenerative disease progression.
Recommended Citation
Ellefson, Erik C., "Wildfire-Derived PM2.5 as a Neuroinflammatory Amplifier of Alzheimer’s and Parkinson’s Disease Pathology: A Narrative Review" (2026). University Honors Theses. Paper 1890.
Included in
Cognitive Neuroscience Commons, Medical Neurobiology Commons, Molecular and Cellular Neuroscience Commons, Other Neuroscience and Neurobiology Commons, Population Health Commons, Quality Improvement Commons