The association between chronic obstructive pulmonary disease and Parkinson’s disease: a nationwide population-based retrospective cohort study

Li, C. H.; Chen, W. C.; Liao, Wei; Tu, Chih‐Yen; Lin, Cheng‐Chieh; Sung, F. C.; Chen, C. H.; Hsu, Wen-Yu

doi:10.1093/qjmed/hcu136

Cited by 44 publications

(36 citation statements)

References 31 publications

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“…In this current study, no association was documented between β2‐agonists and risk of PD. However, COPD patients are intrinsically different from the general population; for one, they have a much higher risk of developing PD compared with the general population 11 ; also, COPD patients use β 2 ‐agonists much more frequently. Such intrinsic differences prevent direct comparison of the current results to those studies.…”

Section: Discussionmentioning

confidence: 99%

“…Due to their pharmacological role in relaxing airway muscles, long‐acting β 2 ‐agonists (LABAs) such as salmeterol and formoterol, provide sustained bronchodilation, while short‐acting β 2 ‐agonists (SABA) such as albuterol, fenoterol and terbutaline, are typically used as rescue medications due to their short duration of action 10 . Being the most prevalent users of β 2 ‐agonists, COPD patients have a 1.4 times higher risk of developing PD 11 possibly due to the impairment of gas exchange and the subsequent hypoxemia and hypercapnia 12 . Therefore, the COPD population may benefit significantly from the neuroprotective effects, if any, of β 2 ‐agonists.…”

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confidence: 99%

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Effects of β2‐Adrenergic Agonists on Risk of Parkinson's Disease in COPD: A Population‐Based Study

et al. 2020

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INTRODUCTION Multiple studies have investigated the role of b 2 -adrenoreceptor agonists on the risk of Parkinson's disease (PD). However, whether b 2 -agonist use is associated with the risk of PD in patients with chronic obstructive pulmonary disease (COPD) has not been examined to date. OBJECTIVES To examine the association between use of b 2 -agonist and the risk of PD in patients with COPD. METHODS A case-control study nested within a cohort of patients with COPD using the British Columbia health administrative databases from 1997 to 2015 was performed. Among a cohort of patients with COPD, all cases of PD were identified, and matched each case to up to five controls by age and calendar time. The use of b 2 -agonists was assessed between the third and fourth year preceding the date of PD diagnosis, followed by additional two years of grace period (between the first and second year preceding PD incidence) to control for PD latency. The use of b 2 -agonists was categorized into three levels: regular use (≥ 1 dispensation for every 6 months), irregular use (dispensation in one to three 6-month periods), and no use. A conditional logistic regression model was used to estimate the rate ratio of PD according to b2-agonist use, rigorously controlling for confounding variables. RESULTS Among 242,218 COPD patients, 732 PD cases and 3660 controls were identified. Use of b 2agonists did not significantly affect the subsequent risk of PD (vs no use, adjusted rate ratios: regular use, 1.14 [95% CI: 0.93, 1.40, p=0.21], irregular use, 1.15 [95% CI: 0.92, 1.45, p=0.22]). Results remained consistent with competing risk sensitivity analysis. CONCLUSION Use of b 2 -agonists does not appear to affect the risk of PD in a real-world COPD population. KEY WORDS COPD, Parkinson's disease, b 2 -agonists, population-based study. (Pharmacotherapy 2020;40(5):408-415)Parkinson's disease (PD) is the second most common neurodegenerative disorder in the world after Alzheimer's disease. 1 Affecting predominantly older persons, PD is prevalent in 1.1% individuals aged 70 to 79 years and 1.9% of individuals older than age 80. 1 As the global population of older adults is projected to reach 425 million by 2050, 2 the burden and morbidity of PD can impose unsustainable demands on limited

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Effects of β2‐Adrenergic Agonists on Risk of Parkinson's Disease in COPD: A Population‐Based Study

et al. 2020

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“…But in contrast, if pulmonary diseases were diagnosed only later in life, an inverse relationship with cognitive impairment was observed [46]. Similarly for other neurodegenerative disorders, a population-based study which evaluated the relationship between COPD and Parkinson's disease found the highest risk for COPD on incident Parkinson's disease in subjects under the age of 65 years [47]. Since incidence rates of neurodegenerative disorders generally increase with age, potential explanations might be that COPD effects are overruled in the course of time by age effects or that elderly with COPD prone to neurodegenerative disorders do not reach high age.…”

Section: Cognitive Impairment (Dementia)mentioning

confidence: 99%

Chronic obstructive pulmonary disease and cerebrovascular disease: A comprehensive review

Lahousse

Tiemeier

Ikram

et al. 2015

Respiratory Medicine

109

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Along with the aging population, the public health burden of cerebrovascular disease is increasing. Cerebral small vessel disease and accumulation of brain pathology associate with cognitive decline and can lead to clinical outcomes, such as stroke and dementia. Chronic Obstructive Pulmonary Disease (COPD) is a common respiratory disease among elderly. The quality of life and prognosis of patients with COPD is greatly determined by the presence of comorbidities including stroke and cognitive impairment. Despite the clinical relevance of cerebral small vessel disease, stroke and (vascular) cognitive impairment in patients with COPD, literature is scarce and underlying mechanisms are unknown. The aim of the present review is therefore to summarize current scientific knowledge, to provide a better understanding of the interplay between COPD and the aging brain and to define remaining knowledge gaps. This narrative review article 1) overviews the epidemiology of cerebral small vessel disease, stroke and cognitive impairment in patients with COPD; 2) discusses potential underlying mechanisms including aging, smoking, systemic inflammation, vasculopathy, hypoxia and genetic susceptibility; and 3) highlights areas requiring further research.

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“…Both PINK1 and PRKN gene mutations associated with mitochondrial dysfunction have been implicated in the development of hereditary recessive early-onset Parkinsonism [8][9][10]. A retrospective cohort study evaluating the clinical connection between Parkinson disease and COPD shows higher risk of developing Parkinson disease in COPD cases [11]. A recent paper demonstrates PRKN deficiency is related to increased inflammation and genomic instability, which can be involved in COPD pathogenesis [12].…”

Section: Introductionmentioning

confidence: 99%

PRKN-regulated mitophagy and cellular senescence during COPD pathogenesis

et al. 2018

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Cigarette smoke (CS)-induced accumulation of mitochondrial damage has been widely implicated in chronic obstructive pulmonary disease (COPD) pathogenesis. Mitophagy plays a crucial role in eliminating damaged mitochondria, and is governed by the PINK1 (PTEN induced putative protein kinase 1)-PRKN (parkin RBR E3 ubiquitin protein ligase) pathway. Although both increased PINK1 and reduced PRKN have been implicated in COPD pathogenesis in association with mitophagy, there are conflicting reports for the role of mitophagy in COPD progression. To clarify the involvement of PRKN-regulated mitophagy in COPD pathogenesis, prkn knockout (KO) mouse models were used. To illuminate how PINK1 and PRKN regulate mitophagy in relation to CS-induced mitochondrial damage and cellular senescence, overexpression and knockdown experiments were performed in airway epithelial cells (AEC). In comparison to wild-type mice, prkn KO mice demonstrated enhanced airway wall thickening with emphysematous changes following CS exposure. AEC in CS-exposed prkn KO mice showed accumulation of damaged mitochondria and increased oxidative modifications accompanied by accelerated cellular senescence. In vitro experiments showed PRKN overexpression was sufficient to induce mitophagy during CSE exposure even in the setting of reduced PINK1 protein levels, resulting in attenuation of mitochondrial ROS production and cellular senescence. Conversely PINK1 overexpression failed to recover impaired mitophagy caused by PRKN knockdown, indicating that PRKN protein levels can be the rate-limiting factor in PINK1-PRKN-mediated mitophagy during CSE exposure. These results suggest that PRKN levels may play a pivotal role in COPD pathogenesis by regulating mitophagy, suggesting that PRKN induction could mitigate the progression of COPD.

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The association between chronic obstructive pulmonary disease and Parkinson’s disease: a nationwide population-based retrospective cohort study

Abstract: This nationwide retrospective cohort study demonstrates that PD risk is significantly increased in patients with COPD compared with those of the general population.

Cited by 44 publications

References 31 publications

Effects of β2‐Adrenergic Agonists on Risk of Parkinson's Disease in COPD: A Population‐Based Study

Effects of β2‐Adrenergic Agonists on Risk of Parkinson's Disease in COPD: A Population‐Based Study

Chronic obstructive pulmonary disease and cerebrovascular disease: A comprehensive review

PRKN-regulated mitophagy and cellular senescence during COPD pathogenesis

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