Association of mild cognitive impairment and characteristic of COPD and overall health status in a cohort study

Yohannes, Abebaw Mengistu; Eakin, Michelle N.; Holbrook, Janet T.; Sugar, Elizabeth A.; Henderson, Robert J.; Baker, Anna M.; Casper, Anne; Kaminsky, David A.; Rea, Alexis; Mathews, Anne M.; Que, Loretta G.; Ramsdell, Joe; Gerald, Lynn B.; Wise, Robert A.; Hanania, Nicola A.

doi:10.1080/17476348.2021.1838278

Cited by 15 publications

(19 citation statements)

References 34 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Some studies have reported 32-37% of people with moderate COPD present with CI [17,42], however the cut-off for CI in the MoCA was much lower when compared to the present study. The higher frequency of CI in our COPD population is in line with a more recent study that identified mild CI in 54% of people with moderate COPD symptoms [43]. In contrast to other studies, we have shown that cognition is not different between people admitted to hospital for an AECOPD and people with stable symptoms [13,14], despite the higher severity of breathlessness and other symptoms in acutely unwell patients.…”

Section: Cognitive Impairment In People With Copdsupporting

confidence: 90%

Cognitive function following pulmonary rehabilitation and post-discharge recovery from exacerbation in people with COPD

Orme

Greening

Steiner

et al. 2021

Respiratory Medicine

View full text Add to dashboard Cite

Background: Cognitive impairment (CI) is prevalent in COPD and is associated with poor health-related quality of life. Recovery of cognition following an acute exacerbation of COPD (AECOPD), the impact of CI on pulmonary rehabilitation (PR) uptake and the effect of PR on CI are not fully understood. Methods: This 6-week prospective study analysed 67 people with stable COPD symptoms who completed PR (PR group) and the recovery of 45 people admitted for AECOPD (AECOPD group). All participants were assessed for cognitive function (Montreal Cognitive Assessment [MoCA]), health status (COPD Assessment Test, Chronic Respiratory Questionnaire), lower extremity function (Short Physical Performance Battery), and psychological well-being (Hospital Anxiety and Depression Score). Follow up assessments were carried out after a 6-week recovery post-discharge in AECOPD group and after PR in the PR group. Results: AECOPD group showed no improvement in MoCA following a 6-week recovery post-discharge (Δ-0.8 ± 3.2, p = 0.205), despite improvements in all other clinical outcomes. PR uptake among the AECOPD group was not associated with the presence of CI (p = 0.325). Participants in the PR group with CI at baseline showed a significant improvement in MoCA score following PR (Δ1.6 ± 2.4, p = 0.004). Conclusions: Cognition does not improve following 6-week recovery post-AECOPD, and CI may influence patients' response to PR referral as an inpatient. PR improves cognition in people with stable COPD symptoms and CI. People with AECOPD should be actively encouraged to attend PR irrespective of mild-moderate cognition but may require additional support or opportunities to take part.

show abstract

Section: Cognitive Impairment In People With Copdsupporting

confidence: 90%

Cognitive function following pulmonary rehabilitation and post-discharge recovery from exacerbation in people with COPD

Orme

Greening

Steiner

et al. 2021

Respiratory Medicine

View full text Add to dashboard Cite

show abstract

“…In addition, studies had different threshold definitions for cognitive impairment, even when using the same cognitive assessment tool. The proportion of coded cognitive impairment at COPD diagnosis in the GP electronic health records presented in this study (3.4%) was far lower than the proportion in clinical studies reported as 40-50% when cognitive impairment was systematically assessed (22,23). This raises a concern of subclinical underdiagnosed cognitive impairment, which may lead to a delayed intervention; and consequently, a missed opportunity to reduce the impact of cognitive impairment on this vulnerable population.…”

Section: Discussioncontrasting

confidence: 66%

Risk of incident dementia and cognitive impairment in patients with chronic obstructive pulmonary disease (COPD): A large UK population-based study

Siraj

McKeever

Gibson

et al. 2021

Respiratory Medicine

View full text Add to dashboard Cite

“…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

View full text Add to dashboard Cite

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

Association of mild cognitive impairment and characteristic of COPD and overall health status in a cohort study

Cited by 15 publications

References 34 publications

Cognitive function following pulmonary rehabilitation and post-discharge recovery from exacerbation in people with COPD

Cognitive function following pulmonary rehabilitation and post-discharge recovery from exacerbation in people with COPD

Risk of incident dementia and cognitive impairment in patients with chronic obstructive pulmonary disease (COPD): A large UK population-based study

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

Contact Info

Product

Resources

About