Ageing and neurodegenerative disease is an emergent public health issue in Taiwan. Particulate air pollution is an important risk factor in cardiopulmonary diseases and neurological disorder; however, the pathophysiology of neurodegenerative diseases occurred by particulate air pollution remains unclear. Our preliminary results showed that pulmonary exposure to diesel exhaust particle (DEP) caused short-term electroencephalography (EEG) alteration and reduction in EEG entropy in Sprague-Dawley (SD) rats. Based on previous epidemiological associations and our preliminary data, we hypothesize that pulmonary exposure to particulate air pollution cause functional change in brain (such as EEG), leading to cognitive dysfunction and development of neurodegenerative diseases. To examine our hypothesis, there are three main objectives in the present study: (1) discover the effects of particulate air pollution on functional changes in brain; (2) explore the roles of particulate air pollution in regulation of cognitive dysfunction; (3) establish the biological evidence in neurodegenerative disease occurred by particulate air pollution. In this 2-year project, aged healthy SD rats and neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced Parkinson’s disease SD rat model (positive control) will be used throughout the study. The rats will be exposed to traffic-related PM2.5 (≤2.5 μm) or HEPA-filtered control (PM2.5 control) for 3 months (1st year) and 6 and 12 months (2nd year) by a whole-body exposure chamber under a consistent humidity and temperature. The whole-body exposure chamber will be set-up in a traffic-dominated area (中和運動中心) and continuously monitored PM2.5 mass and number concentrations as well as gas pollutants (i.e. NOx, SOx and O3). EEG, cognitive functions, behavior and brain MRI will be monitored monthly pre-exposure and during the exposure. The alteration in EEG signals and reduction in complexity in EEG will be calculated. Oxidative stress (i.e. 8-hydroxy-2'-deoxyguanosine), protein oxidation (i.e. carbonyl oxidation), inflammation (i.e. TNF-α, IL-6, NF-kB) and apoptosis (i.e. caspase-3) in brain will be determined. The strength of this study is that we can answer the epidemiological association of particulate air pollution with brain functions and development of neurodegenerative disease based on our toxicological experiment design, which is urgent required for human health protection in aged subjects. Furthermore, EEG is a clinical technique to detect the cognitive function in neurodegenerative disease, which will be applied to the present study. This study can establish the causal relationship between particulate air pollution and neurodegenerative disease, which provides scientific evidence for health improvement in ageing subjects.
|Effective start/end date||8/1/16 → 7/31/17|
- air pollution
- particulate Matter
- neurodegenerative disease