Magnetic resonance apparent diffusion coefficient values of the brain in COPD

Shehata, Mohammad El Desouky Abo; Samaha, Hala Mohamed Shalaby; Elsaid, Amany Ragab; Helmy, Eman; Mustafa, Wessam

doi:10.1016/j.ejcdt.2016.11.003

Cited by 2 publications

(2 citation statements)

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“…COPD-induced neurocognitive dysfunction is an emerging area of research which includes alterations in memory, executive functioning and attention [ 12 – 14 ], with up to 61% of people with COPD suffering from neurocognitive dysfunction [ 12 , 15 , 16 ]. Moreover, neurocognitive dysfunction is associated with much of the disease burden, healthcare utilisation and costs, as people with neurocognitive dysfunction often lack adherence to therapeutic interventions and medication, which in turn worsen their COPD morbidity, lead to increased hospitalisations and risk of mortality [ 12 , 17 ].…”

Section: Introductionmentioning

confidence: 99%

Ebselen prevents cigarette smoke-induced cognitive dysfunction in mice by preserving hippocampal synaptophysin expression

Luca

Brassington

Chan

et al. 2022

J Neuroinflammation

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Background Cigarette smoking (CS) is the leading cause of chronic obstructive pulmonary disease (COPD). The “spill-over” of pulmonary inflammation into the systemic circulation may damage the brain, leading to cognitive dysfunction. Cessation of CS can improve pulmonary and neurocognitive outcomes, however, its benefit on the neuroinflammatory profile remains uncertain. Here, we investigate how CS exposure impairs neurocognition and whether this can be reversed with CS cessation or an antioxidant treatment. Methods Male BALB/c mice were exposed to CS (9 cigarettes/day for 8 weeks) followed by 4 weeks of CS cessation. Another cohort of CS-exposed mice were co-administrated with a glutathione peroxidase mimetic, ebselen (10 mg/kg) or vehicle (5% CM-cellulose). We assessed pulmonary inflammation, spatial and working memory, and the hippocampal microglial, oxidative and synaptic profiles. Results CS exposure increased lung inflammation which was reduced following CS cessation. CS caused spatial and working memory impairments which were attributed to hippocampal microglial activation and suppression of synaptophysin. CS cessation did not improve memory deficits or alter microglial activation. Ebselen completely prevented the CS-induced working and spatial memory impairments, which was associated with restored synaptophysin expression without altering microglial activation. Conclusion We were able to model the CS-induced memory impairment and microglial activation seen in human COPD. The preventative effects of ebselen on memory impairment is likely to be dependent on a preserved synaptogenic profile. Cessation alone also appears to be insufficient in correcting the memory impairment, suggesting the importance of incorporating antioxidant therapy to help maximising the benefit of cessation.

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Section: Introductionmentioning

confidence: 99%

Ebselen prevents cigarette smoke-induced cognitive dysfunction in mice by preserving hippocampal synaptophysin expression

Luca

Brassington

Chan

et al. 2022

J Neuroinflammation

View full text Add to dashboard Cite

show abstract

“…COPD-induced neurocognitive dysfunction is an emerging area of research which includes alterations in memory, executive functioning and attention [12][13][14], with up to 61% of people with COPD suffering from neurocognitive dysfunction [12,15,16]. Moreover, neurocognitive dysfunction is associated with much of the disease burden, healthcare utilization and costs, as people with neurocognitive dysfunction often lack adherence to therapeutic interventions and medication, which in turn worsen their COPD morbidity, lead to increased hospitalizations and risk of mortality [12,17].…”

Section: Introductionmentioning

confidence: 99%

Ebselen Prevents Cigarette Smoke-Induced Cognitive Dysfunction In Mice By Preserving Hippocampal Synaptophysin Expression

Luca

Brassington

Chan

et al. 2021

Preprint

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Background: Cigarette smoking (CS) is the leading cause of chronic obstructive pulmonary disease (COPD). The “spill-over” of pulmonary inflammation into the systemic circulation may damage the brain, leading to cognitive dysfunction. Cessation of CS can improve pulmonary and neurocognitive outcomes, however, its benefit on the neuroinflammatory profile remains uncertain. Here, we investigate how CS exposure impairs neurocognition and whether this can be reversed with CS cessation or an antioxidant treatment. Methods: Male BALB/c mice were exposed CS (9 cigarettes/day for 8 weeks) followed by 4 weeks of CS cessation. Another cohort of CS-exposed mice were co-administrated with a glutathione peroxidase (Gpx) mimetic, ebselen (10mg/kg) or vehicle (5% CM-cellulose). We assessed pulmonary inflammation, spatial and working memory, and the hippocampal microglial, oxidative and synaptic profiles. Results: CS exposure increased lung inflammation which was reduced following CS cessation. CS caused spatial and working memory impairments which were attributed to hippocampal microglial activation and suppression of synaptophysin. CS cessation did not improve memory deficits or alter microglial activation. Ebselen completely prevented the CS-induced working and spatial memory impairments, which was associated with restored synaptophysin expression without altering microglial activation.Conclusion: We were able to model the CS-induced memory impairment and microglial activation seen in human COPD. The preventative effects of ebselen on memory impairment is likely to be dependent on a preserved synaptogenic profile. Cessation alone also appears to be insufficient in correcting the memory impairment, suggesting the importance of incorporating antioxidant therapy to help maximizing the benefit of cessation.

show abstract

Magnetic resonance apparent diffusion coefficient values of the brain in COPD

Cited by 2 publications

References 14 publications

Ebselen prevents cigarette smoke-induced cognitive dysfunction in mice by preserving hippocampal synaptophysin expression

Ebselen prevents cigarette smoke-induced cognitive dysfunction in mice by preserving hippocampal synaptophysin expression

Ebselen Prevents Cigarette Smoke-Induced Cognitive Dysfunction In Mice By Preserving Hippocampal Synaptophysin Expression

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