Ozone pollution, oxidative stress, synaptic plasticity, and neurodegeneration

Area of Science:

• Environmental Health
• Neuroscience
• Toxicology

Background:

• Air pollution, driven by overpopulation and industrial growth, includes ozone, a significant environmental toxin.
• Chronic exposure to low-dose ozone induces oxidative stress, impairing brain function and repair mechanisms.
• This neuroinflammation contributes to the rising incidence of chronic and degenerative diseases.

Purpose of the Study:

• To review the pathophysiological mechanisms linking repeated ozone exposure to neurodegenerative diseases.
• To explore ozone's impact on synaptic plasticity and cognitive processes.
• To elucidate the relationship between air pollution and brain health.

Main Methods:

• Systematic literature search of PubMed, Scopus, and Google Scholar databases.
• Inclusion of original articles and reviews published between 2000 and 2018.
• Focus on studies investigating ozone's effects on synaptic plasticity, cognitive function, and neurodegeneration.

Main Results:

• Ozone exposure leads to chronic oxidative stress, causing loss of dendritic spines and impaired synaptic plasticity.
• Cognitive functions, including learning and memory, are negatively affected by ozone-induced brain alterations.
• Evidence suggests a strong association between chronic ozone exposure and the development and progression of neurodegenerative diseases.

Conclusions:

• Repeated low-dose ozone exposure is a key mechanism driving synaptic plasticity loss via chronic oxidative stress.
• Ozone pollution significantly impacts brain tissue, affecting information processing and neuronal structure.
• A clear link exists between environmental ozone exposure and the onset and advancement of neurodegenerative conditions.