Academic Journal
Cigarette Smoke Exposure Induces Neurocognitive Impairments and Neuropathological Changes in the Hippocampus
| العنوان: | Cigarette Smoke Exposure Induces Neurocognitive Impairments and Neuropathological Changes in the Hippocampus |
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| المؤلفون: | Dobric, Aleksandar, De Luca, Simone N., Seow, Huei Jiunn, Wang, Hao, Brassington, Kurt, Chan, Stanley M. H., Mou, Kevin, Erlich, Jonathan, Liong, Stella, Selemidis, Stavros, Spencer, Sarah J., Bozinovski, Steven, Vlahos, Ross |
| المساهمون: | National Health and Medical Research Council, Australian Lung Foundation, Boehringer Ingelheim |
| المصدر: | Frontiers in Molecular Neuroscience ; volume 15 ; ISSN 1662-5099 |
| بيانات النشر: | Frontiers Media SA |
| سنة النشر: | 2022 |
| المجموعة: | Frontiers (Publisher - via CrossRef) |
| الوصف: | 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. |
| نوع الوثيقة: | article in journal/newspaper |
| اللغة: | unknown |
| DOI: | 10.3389/fnmol.2022.893083 |
| DOI: | 10.3389/fnmol.2022.893083/full |
| الاتاحة: | http://dx.doi.org/10.3389/fnmol.2022.893083 https://www.frontiersin.org/articles/10.3389/fnmol.2022.893083/full |
| Rights: | https://creativecommons.org/licenses/by/4.0/ |
| رقم الانضمام: | edsbas.196BC6EA |
| قاعدة البيانات: | BASE |
| DOI: | 10.3389/fnmol.2022.893083 |
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