Simple non-mydriatic retinal photography is feasible and demonstrates retinal microvascular dilation in Chronic Obstructive Pulmonary Disease (COPD)

McKay, Gareth J.; McCarter, Rachel; Hogg, Ruth; Higbee, Daniel; Bajaj, M-Pk; Burrage, Daniel; Ruickbie, Sachelle; Baker, EH; Jones, Paul; Dodd, James

doi:10.1371/journal.pone.0227175

Cited by 5 publications

(4 citation statements)

References 38 publications

(47 reference statements)

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“…There is evidence that COPD and reduced lung function is associated with micro and macrovascular damage that could mediate the relationship. [30][31][32] It is possible that vascular dementia is causally linked to COPD and lung function, but this outcome was not included in our analysis which was restricted to AD only. Cognitive dysfunction and MCI are well described in COPD.…”

Section: Discussionmentioning

confidence: 99%

Examining the possible causal relationship between lung function, COPD and Alzheimer’s disease: a Mendelian randomisation study

et al. 2021

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RationaleLarge retrospective case-control studies have reported an association between chronic obstructive pulmonary disease (COPD), reduced lung function and an increased risk of Alzheimer’s disease. However, it remains unclear if these diseases are causally linked, or due to shared risk factors. Conventional observational epidemiology suffers from unmeasured confounding and reverse causation. Additional analyses addressing causality are required.ObjectivesTo examine a causal relationship between COPD, lung function and Alzheimer’s disease.MethodsUsing two-sample Mendelian randomisation, we used single nucleotide polymorphisms (SNPs) identified in a genome wide association study (GWAS) for lung function as instrumental variables (exposure). Additionally, we used SNPs discovered in a GWAS for COPD in those with moderate to very severe obstruction. The effect of these SNPs on Alzheimer’s disease (outcome) was taken from a GWAS based on a sample of 24 807 patients and 55 058 controls.ResultsWe found minimal evidence for an effect of either lung function (OR: 1.02 per SD; 95% CI 0.91 to 1.13; p value 0.68) or liability for COPD on Alzheimer’s disease (OR: 0.97 per SD; 95% CI 0.92 to 1.03; p value 0.40).ConclusionNeither reduced lung function nor liability COPD are likely to be causally associated with an increased risk of Alzheimer’s, any observed association is likely due to unmeasured confounding. Scientific attention and health prevention policy may be better focused on overlapping risk factors, rather than attempts to reduce risk of Alzheimer’s disease by targeting impaired lung function or COPD directly.

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Section: Discussionmentioning

confidence: 99%

Examining the possible causal relationship between lung function, COPD and Alzheimer’s disease: a Mendelian randomisation study

et al. 2021

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“…We found no relationships between retinal and kidney microvascular markers and brain MRI markers. This was unexpected, given that previous studies reported retinal microvascular changes in chronic smokers and COPD patients [45,46] and moderate associations between…”

Section: Plos Onementioning

confidence: 79%

Factors affecting brain structure in smoking-related diseases: Chronic Obstructive Pulmonary Disease (COPD) and coronary artery disease

et al. 2021

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Background Changes in brain structure and cognitive decline occur in Chronic Obstructive Pulmonary Disease (COPD). They also occur with smoking and coronary artery disease (CAD), but it is unclear whether a common mechanism is responsible. Methods Brain MRI markers of brain structure were tested for association with disease markers in other organs. Where possible, principal component analysis (PCA) was used to group markers within organ systems into composite markers. Univariate relationships between brain structure and the disease markers were explored using hierarchical regression and then entered into multivariable regression models. Results 100 participants were studied (53 COPD, 47 CAD). PCA identified two brain components: brain tissue volumes and white matter microstructure, and six components from other organ systems: respiratory function, plasma lipids, blood pressure, glucose dysregulation, retinal vessel calibre and retinal vessel tortuosity. Several markers could not be grouped into components and were analysed as single variables, these included brain white matter hyperintense lesion (WMH) volume. Multivariable regression models showed that less well organised white matter microstructure was associated with lower respiratory function (p = 0.028); WMH volume was associated with higher blood pressure (p = 0.036) and higher C-Reactive Protein (p = 0.011) and lower brain tissue volume was associated with lower cerebral blood flow (p<0.001) and higher blood pressure (p = 0.001). Smoking history was not an independent correlate of any brain marker. Conclusions Measures of brain structure were associated with a range of markers of disease, some of which appeared to be common to both COPD and CAD. No single common pathway was identified, but the findings suggest that brain changes associated with smoking-related diseases may be due to vascular, respiratory, and inflammatory changes.

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“…There is evidence that COPD and reduced lung function is associated with micro and macrovascular damage that could mediate the relationship. (31-33) It is possible that vascular dementia is causally linked to COPD and lung function, but this outcome was not included in our analysis which was restricted to Alzheimer’s disease only. Cognitive dysfunction and Mild Cognitive Impairment are well described in COPD (6) .…”

Section: Discussionmentioning

confidence: 99%

Examining the possible causal relationship between Lung Function, COPD and Alzheimer’s Disease. A Mendelian Randomization Study

Higbee¹,

Granell²,

Walton³

et al. 2020

Preprint

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Rationale: Large retrospective case-control studies have reported an association between COPD, reduced lung function and an increased risk of Alzheimers disease. However, it remains unclear if these diseases are causally linked, or due to shared risk factors. Conventional observational epidemiology suffers from unmeasured confounding and reverse causation. Additional analyses addressing causality are required. Objectives: To examine a causal relationship between COPD, lung function and Alzheimers disease. Methods: Using two-sample Mendelian randomization, we utilised single nucleotide polymorphisms (SNPs) identified in a genome wide association study (GWAS) for lung function as instrumental variables (exposure). Additionally, we used SNPs discovered in a GWAS for COPD in those with moderate to very severe obstruction. The effect of these SNPs on Alzheimers disease (outcome) were taken from a GWAS based on a sample of 24,807 patients and 55,058 controls. Results: We found minimal evidence for an effect of either lung function (odds ratio [OR]:1.02 per SD; 95% confidence interval [CI]: 0.91, 1.13; p value 0.68). or liability for COPD on Alzheimers disease (OR: 0.97 per SD; 95% CI: 0.92, 1.03; p value 0.40). Conclusion: Neither reduced lung function nor liability COPD are likely to be causally associated with an increased risk of Alzheimers, any observed association is likely due to unmeasured confounding. Scientific attention and health prevention policy may be better focused on overlapping risk factors, rather than attempts to reduce risk of Alzheimers disease by targeting impaired lung function or COPD directly.

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Simple non-mydriatic retinal photography is feasible and demonstrates retinal microvascular dilation in Chronic Obstructive Pulmonary Disease (COPD)

Cited by 5 publications

References 38 publications

Examining the possible causal relationship between lung function, COPD and Alzheimer’s disease: a Mendelian randomisation study

Examining the possible causal relationship between lung function, COPD and Alzheimer’s disease: a Mendelian randomisation study

Factors affecting brain structure in smoking-related diseases: Chronic Obstructive Pulmonary Disease (COPD) and coronary artery disease

Examining the possible causal relationship between Lung Function, COPD and Alzheimer’s Disease. A Mendelian Randomization Study

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