ArticleFrontiers in molecular neuroscience2022
Cigarette Smoke Exposure Induces Neurocognitive Impairments and Neuropathological Changes in the Hippocampus.
Article in Frontiers in molecular neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 30 citations in OpenAlex.
- Unknotting the crosstalk between COPD and neuroinflammation.Journal of neuroinflammation · 2026Review
- The lung-brain axis: elucidating the mechanisms of pulmonary-driven neurological disorders.Journal of neuroinflammation · 2026Review
- Brain structural changes in COPD patients with cognitive impairment.Journal of neurology · 2026Review
- Cigarette smoke-induced lung-brain barrier dysfunction drives neurocognitive impairment via inflammatory spill-over.Journal of neuroinflammation · 2025Article
- Aberrant brain functional network in COPD patients with cognitive impairment: clinical manifestations, mechanisms and therapeutic strategies.Journal of neuroinflammation · 2025Review
- Memory under siege: the cognitive costs of smoking and vaping.Brain, behavior, & immunity - health · 2025Review
- Nicotine influence on cerebrovascular and neurocognitive function with in utero electronic cigarette exposure.The Journal of physiology · 2025Article
- Observational
- Ivermectin attenuates nicotine-induced reward-like behaviors in mice.Biomolecules & biomedicine · 2025Article
- Partial amelioration of a chronic cigarette-smoke-induced phenotype in mice by switching to electronic cigarettes.Archives of toxicology · 2025Article
- Mesenchymal stem cell-derived exosomes-a promising therapeutic approach to improve neurocognitive disorders in chronic obstructive pulmonary disease.Stem cell research & therapy · 2025Review
- Association Between Smoking and Amnesia in Southwest Iran: A Population-Based Cross-sectional Study.Journal of research in health sciences · 2025Article
- Protective effects of sesamol against cigarette smoke toxicity on the blood-brain barrier.BMC complementary medicine and therapies · 2025Article
- The Lung-Brain Axis in Chronic Obstructive Pulmonary Disease-Associated Neurocognitive Dysfunction: Mechanistic Insights and Potential Therapeutic Options.International journal of biological sciences · 2025Review
- Maternal use of electronic cigarettes and impact on offspring: a double-hit model.Journal of applied physiology (Bethesda, Md. : 1985) · 2024Article
- Review
- Apocynin Prevents Cigarette Smoke-Induced Anxiety-Like Behavior and Preserves Microglial Profiles in Male Mice.Antioxidants (Basel, Switzerland) · 2024Article
- Article
- Targeting accelerated pulmonary ageing to treat chronic obstructive pulmonary disease-induced neuropathological comorbidities.British journal of pharmacology · 2024Review
- miR-153-3p via PIK3R1 Is Involved in Cigarette Smoke-Induced Neurotoxicity in the Brain.Toxics · 2023Article
Corrections and comments
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background and Objective: Neurocognitive dysfunction is present in up to ∼61% of people with chronic obstructive pulmonary disease (COPD), with symptoms including learning and memory deficiencies, negatively impacting the quality of life of these individuals. As the mechanisms responsible for neurocognitive deficits in COPD remain unknown, we explored whether chronic cigarette smoke (CS) exposure causes neurocognitive dysfunction in mice and whether this is associated with neuroinflammation and an altered neuropathology. Methods: Male BALB/c mice were exposed to room air (sham) or CS (9 cigarettes/day, 5 days/week) for 24 weeks. After 23 weeks, mice underwent neurocognitive tests to assess working and spatial memory retention. At 24 weeks, mice were culled and lungs were collected and assessed for hallmark features of COPD. Serum was assessed for systemic inflammation and the hippocampus was collected for neuroinflammatory and structural analysis. Results: Chronic CS exposure impaired lung function as well as driving pulmonary inflammation, emphysema, and systemic inflammation. CS exposure impaired working memory retention, which was associated with a suppression in hippocampal microglial number, however, these microglia displayed a more activated morphology. CS-exposed mice showed changes in astrocyte density as well as a reduction in synaptophysin and dendritic spines in the hippocampus. Conclusion: We have developed an experimental model of COPD in mice that recapitulates the hallmark features of the human disease. The altered microglial/astrocytic profiles and alterations in the neuropathology within the hippocampus may explain the neurocognitive dysfunction observed during COPD.
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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 Socratic graph.