Manja Koch1, Simona Costanzo2, Annette L Fitzpatrick3, Oscar L Lopez4, Steven DeKosky5, Lewis H Kuller6, Julie Price7, Rachel H Mackey6, Majken K Jensen1,8, Kenneth J Mukamal1,9. 1. Department of NutritionHarvard T.H. Chan School of Public Health, Boston, MA, USA. 2. Department of Epidemiology and Prevention, IRCCS Neuromed, Pozzilli (IS), Italy. 3. Departments of Family Medicine, Epidemiology, and Global Health, University of Washington, Seattle, WA, USA. 4. Department of Neurology, School of Medicine, University of Pittsburgh, Pittsburgh, PA, USA. 5. Department of Neurology, University of Florida, Gainesville, FL, USA. 6. Department of Epidemiology, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, PA, USA. 7. Department of Radiology, Massachusetts General Hospital, Boston, MA, USA. 8. Department of Medicine, Channing Division of Network Medicine, Harvard Medical School, Brigham and Women's Hospital, Boston, MA, USA. 9. Department of Medicine, Beth Israel Deaconess Medical Center, Boston, MA, USA.
Abstract
BACKGROUND: Light to moderate alcohol consumption has been variably associated with lower or higher risk of dementia, but effects on Alzheimer's disease pathology are less clear. OBJECTIVE: We determined whether late-life alcohol consumption was associated with Alzheimer's disease pathology among older adults. METHODS: We assessed the associations of alcohol consumption self-reported in 2000-2002 with brain amyloid-β deposition on PET scans, and white matter lesion and hippocampal volume on MRIs measured 7-9 years later in 189 participants of the Ginkgo Evaluation of Memory Study (age 75-87 years at baseline) who were free of clinical dementia, using multivariable-adjusted and inverse probability-weighted robust linear regression models. RESULTS: Alcohol consumption was not statistically significantly associated with amyloid-β deposition (standardized uptake value ratio difference per drink: -0.013 [95% CI: -0.027, 0.002]). Both non-drinkers and participants consuming ≥1 drink(s)/week had higher white matter lesion volume (% intracranial volume) than did the reference group of those consuming <1 drink/week (differences: 0.25 % [95% CI: 0.01, 0.50]; 0.26 % [95% CI: 0.02, 0.50]). The association of alcohol consumption and hippocampal volume was modified by age (p = 0.02). Among participants younger than 77 years, participants consuming 1-7 drinks/week had larger hippocampal volume compared with participants consuming <1 drink/week. CONCLUSIONS: Alcohol consumption was not statistically significantly associated with amyloid-β deposition 7-9 years later. Non-drinking and greater alcohol consumption were associated with higher white matter lesion volume compared with drinking <1 drink/week. Moderate drinking was associated with higher hippocampal volume in younger individuals. Given the selective nature of this population and adverse health effects of excessive alcohol consumption, these findings warrant further investigation, but cannot be translated into clinical recommendations.
BACKGROUND: Light to moderate alcohol consumption has been variably associated with lower or higher risk of dementia, but effects on Alzheimer's disease pathology are less clear. OBJECTIVE: We determined whether late-life alcohol consumption was associated with Alzheimer's disease pathology among older adults. METHODS: We assessed the associations of alcohol consumption self-reported in 2000-2002 with brain amyloid-β deposition on PET scans, and white matter lesion and hippocampal volume on MRIs measured 7-9 years later in 189 participants of the Ginkgo Evaluation of Memory Study (age 75-87 years at baseline) who were free of clinical dementia, using multivariable-adjusted and inverse probability-weighted robust linear regression models. RESULTS:Alcohol consumption was not statistically significantly associated with amyloid-β deposition (standardized uptake value ratio difference per drink: -0.013 [95% CI: -0.027, 0.002]). Both non-drinkers and participants consuming ≥1 drink(s)/week had higher white matter lesion volume (% intracranial volume) than did the reference group of those consuming <1 drink/week (differences: 0.25 % [95% CI: 0.01, 0.50]; 0.26 % [95% CI: 0.02, 0.50]). The association of alcohol consumption and hippocampal volume was modified by age (p = 0.02). Among participants younger than 77 years, participants consuming 1-7 drinks/week had larger hippocampal volume compared with participants consuming <1 drink/week. CONCLUSIONS:Alcohol consumption was not statistically significantly associated with amyloid-β deposition 7-9 years later. Non-drinking and greater alcohol consumption were associated with higher white matter lesion volume compared with drinking <1 drink/week. Moderate drinking was associated with higher hippocampal volume in younger individuals. Given the selective nature of this population and adverse health effects of excessive alcohol consumption, these findings warrant further investigation, but cannot be translated into clinical recommendations.
Entities:
Keywords:
Alcohol; brain amyloid-βzzm321990; epidemiology; hippocampal volume; white matter lesions
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