Distinct brain lipid signatures in response to low-level PM exposure in a 3xTg-Alzheimer's disease mouse inhalation model.

Sci Total Environ

Institute of Environmental and Occupational Health Sciences, College of Public Health, National Taiwan University, Taipei, Taiwan; Department of Public Health, National Taiwan University, Taipei, Taiwan. Electronic address:

Published: September 2022

AI Article Synopsis

  • Fine particulate matter (PM) is harmful to human health, and its effects on brain function and structure, particularly in Alzheimer's disease, are not well understood.
  • In a study involving 3xTg-Alzheimer’s disease mice, exposure to low levels of PM over three months led to notable changes in lipid profiles in several brain areas, indicating potential neurotoxicity.
  • The findings highlight that subchronic PM exposure may disrupt lipid metabolism, which could contribute to Alzheimer's development, suggesting lipidomics could be essential for studying early PM-related brain toxicity.

Article Abstract

Fine particulate matter (PM) poses a significant risk to human health. The molecular mechanisms underlying low-level PM-induced neurotoxicity in the central nervous system remain unclear. In addition, changes in lipids in response to PM exposure have not yet been fully elucidated. In this study, 3xTg-Alzheimer's disease (AD) mice experienced continuous whole-body exposure to non-concentrated PM for three consecutive months, while control mice inhaled particulate matter-filtered air over the same time span. A liquid chromatography-mass spectrometry-based lipidomic platform was used to determine the distinct lipid profiles of various brain regions. The average PM concentration during the exposure was 11.38 μg/m, which was close to the regulation limits of USA and Taiwan. The partial least squares discriminant analysis model showed distinct lipid profiles in the cortex, hippocampus, and olfactory bulb, but not the cerebellum, of mice in the exposure group. Increased levels of fatty acyls, glycerolipids, and sterol lipids, as well as the decreased levels of glycerophospholipids and sphingolipids in PM-exposed mouse brains may be responsible for the increased energy demand, membrane conformation, neuronal loss, antioxidation, myelin function, and cellular signaling pathways associated with AD development. Our research suggests that subchronic exposure to low levels of PM may cause neurotoxicity by changing the lipid profiles in a susceptible model. Lipidomics is a powerful tool to study the early effects of PM-induced AD toxicity.

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Source
http://dx.doi.org/10.1016/j.scitotenv.2022.156456DOI Listing

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