Key result
COPD was associated with significantly worse cognitive function (p=0.011), lower mood (p=0.046), and greater gray matter atrophy (p=0.020) compared to non-COPD controls with >10 pack-years smoking.
Why the study?
Cardiovascular risk factors and smoking contribute to neurodegeneration, but whether COPD causes specific deterioration in brain structure and function independent of these factors was unknown.
Does COPD cause deterioration in brain structure and function independent of cardiovascular risk factors and smoking compared to non-COPD smokers?
Case-Control (n=50)
Does COPD cause deterioration in brain structure and function independent of cardiovascular risk factors and smoking compared to non-COPD smokers?
p-value: p=0.011, 0.046, 0.020
COPD is associated with structural and functional brain changes that are independent of cardiovascular risk, aortic stiffness, or smoking history.
Supports COPD-related cognitive and structural brain changes beyond smoking; leaves open causality and practice implications.
Background: Brain damage and cardiovascular disease are extra-pulmonary manifestations of chronic obstructive pulmonary disease (COPD). Cardiovascular risk factors and smoking are contributors to neurodegeneration. This study investigates whether there is a specific, COPD-related deterioration in brain structure and function independent of cardiovascular risk factors and smoking. Materials and methods: Neuroimaging and clinical markers of brain structure (micro- and macro-) and function (cognitive function and mood) were compared between 27 stable COPD patients (age: 63.0±9.1 years, 59.3% male, forced expiratory volume in 1 second [FEV 1 ]: 58.1±18.0% pred.) and 23 non-COPD controls with >10 pack years smoking (age: 66.6±7.5 years, 52.2% male, FEV 1 : 100.6±19.1% pred.). Clinical relationships and group interactions with brain structure were also tested. All statistical analyses included correction for cardiovascular risk factors, smoking, and aortic stiffness. Results: COPD patients had significantly worse cognitive function ( p= 0.011), lower mood ( p= 0.046), and greater gray matter atrophy ( p =0.020). In COPD patients, lower mood was associated with markers of white matter (WM) microstructural damage ( p <0.001), and lower lung function (FEV 1 /forced vital capacity and FEV 1 ) with markers of both WM macro ( p =0.047) and microstructural damage ( p =0.028). Conclusion: COPD is associated with both structural (gray matter atrophy) and functional (worse cognitive function and mood) brain changes that cannot be explained by measures of cardiovascular risk, aortic stiffness, or smoking history alone. These results have important implications to guide the development of new interventions to prevent or delay progression of neuropsychiatric comorbidities in COPD. Relationships found between mood and microstructural abnormalities suggest that in COPD, anxiety, and depression may occur secondary to WM damage. This could be used to better understand disabling symptoms such as breathlessness, improve health status, and reduce hospital admissions.
No takes yet. Share an insight, caveat, or question.
Spilling et al. (2019) conducted a case-control in Chronic obstructive pulmonary disease (COPD) (n=50). COPD vs. Non-COPD controls with >10 pack years smoking was evaluated on Neuroimaging and clinical markers of brain structure (micro- and macro-) and function (cognitive function and mood) (p=0.011, 0.046, 0.020). COPD was associated with significantly worse cognitive function (p=0.011), lower mood (p=0.046), and greater gray matter atrophy (p=0.020) compared to non-COPD controls with >10 pack-years smoking.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: