Core Viewpoint - Long-term exposure to air pollutants, specifically PM2.5, significantly increases the risk of Lewy body dementia (LBD), highlighting the need for further research on air pollution's role in neurodegenerative diseases and its implications for public health strategies [4][11]. Group 1: Research Findings - A large-scale study involving 56 million individuals indicates a strong association between long-term PM2.5 exposure and hospitalization due to α-synucleinopathies, particularly in patients with LBD compared to those with non-dementia Parkinson's disease [4][7]. - The study demonstrates that α-synuclein plays a critical role in PM2.5-related neurodegenerative diseases, with wild-type mice exposed to PM2.5 for 10 months showing brain atrophy, cognitive deficits, and widespread α-synuclein pathology [8][11]. - PM2.5 exposure induces a pathogenic variant of α-synuclein, termed PM-PFF, which exhibits characteristics similar to those found in human LBD, including accelerated aggregation and increased neurotoxicity [8][11]. Group 2: Mechanisms and Implications - Chronic PM2.5 exposure and PM-PFF inoculation in humanized α-synuclein mice trigger gene expression changes that resemble those in LBD patients, underscoring a specific pathogenic axis for LBD [9][11]. - The findings suggest that PM-PFF could serve as a potential therapeutic target, emphasizing the importance of understanding environmental mechanisms in the pathogenesis of LBD [11].