ArticleAlzheimer's & dementia : the journal of the Alzheimer's Association2024
Transcriptomic and epigenomic profiling reveals altered responses to diesel emissions in Alzheimer's disease both in vitro and in population-based data.
Article in Alzheimer's & dementia : the journal of the Alzheimer's Association, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Urban PMMolecular neurobiology · 2026Article
- Olfactory-Cleft Biopsy in Alzheimer's Disease: An Emerging Neuroimmune Window into Preclinical Pathobiology.International journal of molecular sciences · 2026Review
- Analyzing the global burden of 11 subtypes of congenital birth defects: trends, sociodemographic correlates, and outcomes from 1990 to 2021.Annals of medicine · 2025Article
- Impact of air pollution and occupational inhalation exposures on neurodegenerative disorders: An epigenetic perspective.iScience · 2025Review
- Transcriptomic and epigenomic profiling reveals altered responses to diesel emissions in Alzheimer's disease both in vitro and in population-based data.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
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Abstract
introductionStudies have correlated living close to major roads with Alzheimer's disease (AD) risk. However, the mechanisms responsible for this link remain unclear.
methodsWe exposed olfactory mucosa (OM) cells of healthy individuals and AD patients to diesel emissions (DE). Cytotoxicity of exposure was assessed, mRNA, miRNA expression, and DNA methylation analyses were performed. The discovered altered pathways were validated using data from the human population-based Rotterdam Study.
resultsDE exposure resulted in an almost four-fold higher response in AD OM cells, indicating increased susceptibility to DE effects. Methylation analysis detected different DNA methylation patterns, revealing new exposure targets. Findings were validated by analyzing data from the Rotterdam Study cohort and demonstrated a key role of nuclear factor erythroid 2-related factor 2 signaling in responses to air pollutants. DISCUSSION: This study identifies air pollution exposure biomarkers and pinpoints key pathways activated by exposure. The data suggest that AD individuals may face heightened risks due to impaired cellular defenses. HIGHLIGHTS: Healthy and AD olfactory cells respond differently to DE exposure. AD cells are highly susceptible to DE exposure. The NRF2 oxidative stress response is highly activated upon air pollution exposure. DE-exposed AD cells activate the unfolded protein response pathway. Key findings are also confirmed in a population-based study.
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