Affiliation:
1. Aging Research Center Department of Neurobiology Care Sciences and Society Karolinska Institutet and Stockholm University Stockholm Sweden
2. Stockholm Gerontology Research Centre Stockholm Sweden
3. Department of Medical Sciences University of Ferrara Ferrara Italy
4. Unit of Epidemiology Institute of Environmental Medicine Karolinska Institutet Stockholm Sweden
Abstract
AbstractBACKGROUNDWe investigated the association of peak expiratory flow (PEF) with dementia; cognitive impairment, no dementia (CIND); and transition from CIND to dementia, and possible underlying neuropathological mechanisms.METHODSA population‐based cohort of adults aged 60+ was followed over 15 years to detect dementia (Diagnostic and Statistical Manual of Mental Disorders, 4th edition criteria), CIND (assessed through a cognitive battery), and progression from CIND to dementia, in relation to baseline PEF observations. A subsample (n = 462) had 6‐year follow‐up data on brain magnetic resonance imaging markers of neurodegeneration and small vessel disease.RESULTSIn fully adjusted models, poor PEF performance (< 10th vs. ≥ 80th percentile) was associated with increased hazards for dementia (hazard ratio [HR] = 1.89; 95% confidence interval [CI] = 1.23–2.92) and CIND (HR = 1.55; 95% CI = 1.01–2.38) and CIND progression to dementia, although not statistically significantly (HR = 2.44; 95% CI = 0.78–6.88). People with poor PEF also experienced the fastest ventricular enlargement (β coefficient = 0.67 mL/year; 95% CI = 0.13–1.21) and had the highest likelihood of developing lacunes (odds ratio = 5.05; 95% CI = 1.01–25.23).DISCUSSIONPoor lung function contributes to cognitive deterioration possibly through accelerated brain atrophy and microvascular damage.Highlights
Poor lung function increased the risk of dementia and mild cognitive impairment (MCI).
Poor lung function accelerated the progression from MCI to dementia.
Poor lung function was linked to brain microvascular damage and global brain atrophy.