ArticlePloS one2015
Gulf War agent exposure causes impairment of long-term memory formation and neuropathological changes in a mouse model of Gulf War Illness.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 77 citations in OpenAlex.
- Gulf War Illness: Neurological Impacts, Pathophysiological Insights, and Therapeutic Prospects.Molecular neurobiology · 2026Review
- Association between insecticide exposomics and cognitive function in older adults: an observational study based on NHANES 2011-2014.Frontiers in public health · 2025Observational
- Crisis in the gut: navigating gastrointestinal challenges in Gulf War Illness with bioengineering.Military Medical Research · 2024Review
- Exposure to Gulf war illness-related chemicals exacerbates alcohol-induced liver damage in rodents.Scientific reports · 2024Article
- Exposure to Gulf war illness-related chemicals exacerbates alcohol- induced liver damage in rodents.Research square · 2024Article
- Longitudinal evaluation of structural brain alterations in two established mouse models of Gulf War Illness.Frontiers in neuroscience · 2024Article
- Exposing the latent phenotype of Gulf War Illness: examination of the mechanistic mediators of cognitive dysfunction.Frontiers in immunology · 2024Review
- Gulf war toxicant-induced effects on the hippocampal dendritic arbor are reversed by treatment with aFrontiers in neuroscience · 2024Article
- Delayed cognitive impairments in a rat model of Gulf War Illness are stimulus-dependent.Brain, behavior, and immunity · 2023Article
- Pathophysiological basis and promise of experimental therapies for Gulf War Illness, a chronic neuropsychiatric syndrome in veterans.Psychopharmacology · 2023Review
- Chemical exposures and suspected impact on Gulf War Veterans.Military Medical Research · 2023Article
- Impact of gulf war toxic exposures after mild traumatic brain injury.Acta neuropathologica communications · 2022Article
- Pyridostigmine bromide elicits progressive and chronic impairments in the cholinergic anti-inflammatory pathway in the prefrontal cortex and hippocampus of male rats.Neurobiology of stress · 2022Article
- Oral Nano-Curcumin in a Model of Chronic Gulf War Illness Alleviates Brain Dysfunction with Modulation of Oxidative Stress, Mitochondrial Function, Neuroinflammation, Neurogenesis, and Gene Expression.Aging and disease · 2022Article
- Persistent exercise fatigue and associative learning deficits in combination with transient glucose dyshomeostasis in a mouse model of Gulf War Illness.Life sciences · 2022Article
- Brain-Specific Increase in Leukotriene Signaling Accompanies Chronic Neuroinflammation and Cognitive Impairment in a Model of Gulf War Illness.Frontiers in immunology · 2022Article
- Veteran-derived cerebral organoids display multifaceted pathological defects in studies on Gulf War Illness.Frontiers in cellular neuroscience · 2022Article
- Gene-Toxicant Interactions in Gulf War Illness: Differential Effects of theBrain sciences · 2021Article
- Neuroimmune mechanisms of cognitive impairment in a mouse model of Gulf War illness.Brain, behavior, and immunity · 2021Article
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Corrections and comments
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gulf War Illness (GWI) is a chronic multisymptom illness with a central nervous system component such as memory deficits, neurological, and musculoskeletal problems. There are ample data that demonstrate that exposure to Gulf War (GW) agents, such as pyridostigmine bromide (PB) and pesticides such as permethrin (PER), were key contributors to the etiology of GWI post deployment to the Persian GW. In the current study, we examined the consequences of acute (10 days) exposure to PB and PER in C57BL6 mice. Learning and memory tests were performed at 18 days and at 5 months post-exposure. We investigated the relationship between the cognitive phenotype and neuropathological changes at short and long-term time points post-exposure. No cognitive deficits were observed at the short-term time point, and only minor neuropathological changes were detected. However, cognitive deficits emerged at the later time point and were associated with increased astrogliosis and reduction of synaptophysin staining in the hippocampi and cerebral cortices of exposed mice, 5 months post exposure. In summary, our findings in this mouse model of GW agent exposure are consistent with some GWI symptom manifestations, including delayed onset of symptoms and CNS disturbances observed in GWI veterans.
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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.