Vladimir A. Popov, Svetlana Ukraintseva, Hongzhe Duan, Arseniy Yashkin, Julia Kravchenko, Igor Akushevich, Heather Whitson, Konstantin G. Arbeev, Anatoliy I. Yashin

Traffic-related air pollution significantly aggravates the detrimental effect of infections on the risk of Alzheimer’s disease and other dementias, especially in non-carriers of APOE4

Introduction

Traffic-related air pollution significantly aggravates the detrimental effect of infections on the risk of alzheimer’s disease and other dementias, especially in non-carriers of apoe4. Discover how traffic-related air pollution intensifies the link between infections and Alzheimer's/dementia risk, particularly in individuals without the APOE4 gene.

Abstract

Review

This study presents a compelling and timely contribution to our understanding of Alzheimer's disease and other dementias, highlighting a critical interplay between environmental pollution and infectious burden. The central finding – that traffic-related air pollution (TRAP) significantly *aggravates* the detrimental effect of infections on dementia risk – underscores the complex, multifactorial etiology of these neurodegenerative conditions. Particularly striking is the observation that this synergistic effect is most pronounced in non-carriers of the APOE4 allele, suggesting a distinct pathway or heightened vulnerability for individuals not traditionally considered at high genetic risk for late-onset AD. This work strongly implies that public health strategies must consider the combined impact of environmental and biological stressors. The research's strength lies in its ability to identify a novel and potent interaction between two widespread factors known individually to impact health: air pollution and infections. By demonstrating a synergistic effect, the study moves beyond simplistic risk factor analysis to a more integrated view of disease pathogenesis. The specific emphasis on APOE4 non-carriers is a significant asset, as it sheds light on a demographic often overlooked in APOE4-centric research, potentially revealing critical pathways of neurodegeneration independent of this major genetic risk factor. This suggests the study likely employs robust epidemiological methods capable of disentangling complex exposure histories and health outcomes over time within a large population cohort. While the abstract provides a powerful summary, a full review would benefit from details on the study's methodology, including the specific types of infections investigated, the measures of TRAP exposure, and the follow-up duration. Future research building upon these findings should aim to elucidate the precise biological mechanisms underlying this synergy, perhaps exploring how TRAP exposure alters immune responses to infections or exacerbates neuroinflammation, particularly in APOE4 non-carriers. Nevertheless, this work offers a crucial public health message, emphasizing the importance of improving air quality and mitigating infection risks as potential strategies to reduce the burden of dementia, particularly for individuals without a genetic predisposition from APOE4.

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