ArticleToxicological sciences : an official journal of the Society of Toxicology2015
Cyclic Ozone Exposure Induces Gender-Dependent Neuropathology and Memory Decline in an Animal Model of Alzheimer's Disease.
Article in Toxicological sciences : an official journal of the Society of Toxicology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
19 citing papers in PubMed, 35 citations in OpenAlex.
- Neuronal and Astrocytic Lipid Metabolic Coupling Mediates Ozone-Induced Learning and Memory Impairment.Environment & health (Washington, D.C.) · 2026Article
- Age- and ApoE Genotype-Dependent Transcriptomic Responses to OInternational journal of molecular sciences · 2025Article
- Association of Gaseous Ambient Air Pollution and Dementia-Related Neuroimaging Markers in the ARIC Cohort, Comparing Exposure Estimation Methods and Confounding by Study Site.Environmental health perspectives · 2024Article
- Peripheral HMGB1 is linked to OAlzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
- Nitrooxidative Stress and Neuroinflammation Caused by Air Pollutants Are Associated with the Biological Markers of Neurodegenerative Diseases.Antioxidants (Basel, Switzerland) · 2024Review
- Acute Ozone-Induced Transcriptional Changes in Markers of Oxidative Stress and Glucocorticoid Signaling in the Rat Hippocampus and Hypothalamus Are Sex-Specific.International journal of molecular sciences · 2023Article
- The bidirectional lung brain-axis of amyloid-β pathology: ozone dysregulates the peri-plaque microenvironment.Brain : a journal of neurology · 2023Article
- The Effects of Chronic Exposure to Ambient Traffic-Related Air Pollution on Alzheimer's Disease Phenotypes in Wildtype and Genetically Predisposed Male and Female Rats.Environmental health perspectives · 2021Article
- Association Between Ambient Air Pollution and Amyloid Positron Emission Tomography Positivity in Older Adults With Cognitive Impairment.JAMA neurology · 2021Article
- A mechanistic view on the neurotoxic effects of air pollution on central nervous system: risk for autism and neurodegenerative diseases.Environmental science and pollution research international · 2021Review
- Cyclic ONeurobiology of aging · 2019Article
- Dietary Curcumin Prevented Astrocytosis, Microgliosis, and Apoptosis Caused by Acute and Chronic Exposure to Ozone.Molecules (Basel, Switzerland) · 2019Article
- PMToxicology research · 2019Article
- Sex-Specific Differences in Redox Homeostasis in Brain Norm and Disease.Journal of molecular neuroscience : MN · 2019Review
- Aging Exacerbates Neuroinflammatory Outcomes Induced by Acute Ozone Exposure.Toxicological sciences : an official journal of the Society of Toxicology · 2018Article
- At seeming safe concentrations, synergistic effects of PMOncotarget · 2017Article
- Intracranial IL-17A overexpression decreases cerebral amyloid angiopathy by upregulation of ABCA1 in an animal model of Alzheimer's disease.Brain, behavior, and immunity · 2017Article
- Serum amyloid A: an ozone-induced circulating factor with potentially important functions in the lung-brain axis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017Article
- Acute Ozone-Induced Pulmonary and Systemic Metabolic Effects Are Diminished in Adrenalectomized Rats.Toxicological sciences : an official journal of the Society of Toxicology · 2016Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Alzheimer's disease (AD) is a major cause of dementia in the elderly. Although early-onset (familial) AD is attributed to gene mutations, the cause for late-onset (sporadic) AD, which accounts for 95% of AD cases, is unknown. In this study, we show that exposure of 6-week-old amyloid beta precursor protein (APP)/presenilin (PS1) overexpressing mice, a well-established animal model of AD, and nontransgenic littermates to a cyclic O3 exposure protocol, which mimics environmental exposure episodes, accelerated learning/memory function loss in male APP/PS1 mice but not in female APP/PS1 mice or nontransgenic littermates. Female APP/PS1 mice had higher brain levels of amyloid beta peptide (Aβ42) and Aβ40, compared with male APP/PS1 mice; O3 exposure, however, had no significant effect on brain Aβ load in either male or female mice. Our results further show that male APP/PS1 mice had lower levels of antioxidants (glutathione and ascorbate) and experienced augmented induction of NADPH oxidases, lipid peroxidation, and neuronal apoptosis upon O3 exposure, compared with female APP/PS1 mice. No significant effect of O3 on any of these parameters was detected in nontransgenic littermates. In vitro studies further show that 4-hydroxynonenal, a lipid peroxidation product which was increased in the plasma and cortex/hippocampus of O3-exposed male APP/PS1 mice, induced neuroblastoma cell apoptosis. Together, the results suggest that O3 exposure per se may not cause AD but can synergize with genetic risk factors to accelerate the pathophysiology of AD in genetically predisposed populations. The results also suggest that males may be more sensitive to O3-induced neuropathophysiology than females due to lower levels of antioxidants.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.