The pathogenic effects of particulate matter on neurodegeneration: a review

Abstract

The increasing amount of particulate matter (PM) in the ambient air is a pressing public health issue globally. Epidemiological studies involving data from millions of patients or volunteers have associated PM with increased risk of dementia and Alzheimer’s disease in the elderly and cognitive dysfunction and neurodegenerative pathology across all age groups, suggesting that PM may be a risk factor for neurodegenerative diseases. Neurodegenerative diseases affect an increasing population in this aging society, putting a heavy burden on economics and family. Therefore, understanding the mechanism by which PM contributes to neurodegeneration is essential to develop effective interventions. Evidence in human and animal studies suggested that PM induced neurodenegerative-like pathology including neurotoxicity, neuroinflammation, oxidative stress, and damage in blood–brain barrier and neurovascular units, which may contribute to the increased risk of neurodegeneration. Interestingly, antagonizing oxidative stress alleviated the neurotoxicity of PM, which may underlie the essential role of oxidative stress in PM’s potential effect in neurodegeneration. This review summarized up-to-date epidemiological and experimental studies on the pathogenic role of PM in neurodegenerative diseases and discussed the possible underlying mechanisms.

A comprehensive understanding of ambient particulate matter and its components on the adverse health effects based from epidemiological and laboratory evidence

“…Previous reviews have preliminary illustrated relevant mechanisms from the perspective of PM-related cell death patterns or the perspective of certain diseases or systems, pointing out that oxidative stress, inflammation, apoptosis, autophagy and DNA damage are the main mechanisms leading to the adverse effects of PM [12,[22][23][24]. In vitro and in vivo studies have shown that PM 2.5 causes oxidative stress through the induction of reactive oxygen species (ROS), which leads to dysregulation of calcium homeostasis and cytotoxicity [25,26].…”

Neuro‐Glia‐Vascular‐on‐a‐Chip System to Assess Aggravated Neurodegeneration via Brain Endothelial Cells upon Exposure to Diesel Exhaust Particles

“…PM invades brain tissue via direct transmission through the nasal epithelium and olfactory receptor neurons [ 7 ] or blood circulation. [ 8 ] A previous post‐mortem study showed that magnetic nanoparticles were observed in the brain tissues obtained from all 38 cases, [ 9 ] indicating that PM had penetrated the brain. Individuals exposed to PM show several notable features, such as impaired brain development, cognitive deficits, inflammation in the blood–brain barrier (BBB), and the accumulation of neurotoxic protein aggregates.…”

“…Individuals exposed to PM show several notable features, such as impaired brain development, cognitive deficits, inflammation in the blood-brain barrier (BBB), and the accumulation of neurotoxic protein aggregates. [8] The exposure of brain tissue to PM has a negative effect on the central nervous system (CNS) and can cause dementia, [10] stroke, [11] depression, [12] and schizophrenia. [13] To investigate PM toxicity, 2D culture systems and animal models have been widely used.…”

Emissions of Carbonaceous Particulate Matter and Ultrafine Particles from Vehicles—A Scientific Review in a Cross-Cutting Context of Air Pollution and Climate Change

“…Harmful systemic health effects of PM 10 or PM 2.5 are often attributable to the UFP fraction. According to recent works [ 181 , 182 ], exposure to combustion-generated ultrafine particles and engineered nanoparticles can also be linked to neurodegenerative diseases documented in young, urbanised residents of polluted cities.…”