神经炎症
氧化应激
小胶质细胞
疾病
医学
帕金森病
机制(生物学)
神经科学
多发性硬化
神经毒性
炎症
免疫学
环境卫生
生物
病理
毒性
内科学
哲学
认识论
作者
Jian Wang,Tengfei Ma,Ding Ma,Huimin Li,Hua Li,Qing He,Xiaobei Deng
标识
DOI:10.1097/ftd.0000000000000818
摘要
Background: With the development of industrialization in human society, ambient pollutants are becoming more harmful to human health. Epidemiological and toxicological studies indicate that a close relationship exists between particulate matter with a diameter ≤2.5 µm (PM 2.5 ) and neurodegenerative diseases such as Alzheimer's disease (AD) and Parkinson's disease (PD). To further confirm the relationship, we focus on possible relevant mechanisms of oxidative stress and neuroinflammation underlying the association between PM 2.5 and neurodegenerative diseases in the review. Methods: A literature search was performed on the studies about PM 2.5 and neurodegenerative diseases via PubMed. A total of 113 articles published were selected, and 31 studies were included. Results: PM 2.5 can enter the central nervous system through 2 main pathways, the blood–brain barrier and olfactory neurons. The inflammatory response and oxidative stress are 2 primary mechanisms via which PM 2.5 leads to toxicity in the brain. PM 2.5 abnormally activates microglia, inducing the neuroinflammatory process. Inflammatory markers such as IL-1β play an essential role in neurodegenerative diseases such as AD and PD. Moreover, the association between lipid mechanism disorders related to PM 2.5 and neurodegenerative diseases has been gaining momentum. Conclusions: In conclusion, PM 2.5 could significantly increase the risk of neurological disorders, such as AD and PD. Furthermore, any policy aimed at reducing air-polluting emissions and increasing air quality would be protective in human beings.
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