한빛사논문
- 조회1,900
Jee Wook Kim1,2, Min Soo Byun3, Dahyun Yi3, Jun Ho Lee4, Kang Ko5, So Yeon Jeon6, Bo Kyung Sohn7, Jun-Young Lee8,9, Yu Kyeong Kim10, Seong A Shin10, Chul-Ho Sohn11, Dong Young Lee3,4,9,*, for the KBASE Research Group¶
1 Department of Neuropsychiatry, Hallym University Dongtan Sacred Heart Hospital, Hwaseong, Republic of Korea, 2 Department of Psychiatry, Hallym University College of Medicine, Chuncheon, Republic of Korea, 3 Institute of Human Behavioral Medicine, Medical Research Center, Seoul National University, Seoul, Republic of Korea, 4 Department of Neuropsychiatry, Seoul National University Hospital, Seoul, Republic of Korea, 5 Department of Geriatric Psychiatry, National Center for Mental Health, Seoul, Republic of Korea, 6 Department of Psychiatry, Chungnam National University Hospital, Daejeon, Republic of Korea, 7 Department of Psychiatry, Sanggye Paik Hospital, Inje University College of Medicine, Seoul, Republic of Korea, 8 Department of Neuropsychiatry, SMG-SNU Boramae Medical Center, Seoul, Republic of Korea, 9 Department of Psychiatry, Seoul National University College of Medicine, Seoul, Republic of Korea, 10 Department of Nuclear Medicine, SMG-SNU Boramae Medical Center, Seoul, Republic of Korea, 11 Department of Radiology, Seoul National University College of Medicine, Seoul, Republic of Korea
¶ Membership of the KBASE Research Group is provided in the Acknowledgments.
*To whom correspondence should be addressed.
Abstract
Background
An emerging body of literature has indicated that moderate alcohol intake may be protective against Alzheimer disease (AD) dementia. However, little information is available regarding whether moderate alcohol intake is related to reductions in amyloid-beta (Aβ) deposition, or is protective via amyloid-independent mechanisms in the living human brain. Here we examined the associations of moderate alcohol intake with in vivo AD pathologies, including cerebral Aβ deposition, neurodegeneration of AD-signature regions, and cerebral white matter hyperintensities (WMHs) in the living human brain.
Methods and findings
The present study was part of the Korean Brain Aging Study for Early Diagnosis and Prediction of Alzheimer’s Disease (KBASE), an ongoing prospective cohort study that started in 2014. As of November 2016, 414 community-dwelling individuals with neither dementia nor alcohol-related disorders (280 cognitively normal [CN] individuals and 134 individuals with mild cognitive impairment [MCI]) between 56 and 90 years of age (mean age 70.9 years ± standard deviation 7.8; male, n [%] = 180 [43.5]) were recruited from 4 sites (i.e., 2 university hospitals and 2 public centers for dementia prevention and management) around Seoul, South Korea. All the participants underwent comprehensive clinical assessments comprising lifetime and current histories of alcohol intake and multimodal brain imaging, including [11C] Pittsburgh compound B positron emission tomography (PET), [18F] fluorodeoxyglucose (FDG) PET, and magnetic resonance imaging (MRI) scans. Lifetime and current alcohol intake were categorized as follows: no drinking, <1 standard drink (SD)/week, 1–13 SDs/week, and 14+ SDs/week. A moderate lifetime alcohol intake (1–13 SDs/week) was significantly associated with a lower Aβ positivity rate compared to the no drinking group, even after controlling for potential confounders (odds ratio 0.341, 95% confidence interval 0.163–0.714, p = 0.004). In contrast, current alcohol intake was not associated with amyloid deposition. Additionally, alcohol intake was not related to neurodegeneration of AD-signature regions or cerebral WMH volume. The present study had some limitations in that it had a cross-sectional design and depended on retrospective recall for alcohol drinking history.
Conclusions
In this study, we observed in middle- and old-aged individuals with neither dementia nor alcohol-related disorders that moderate lifetime alcohol intake was associated with lower cerebral Aβ deposition compared to a lifetime history of not drinking. Moderate lifetime alcohol intake may have a beneficial influence on AD by reducing pathological amyloid deposition rather than amyloid-independent neurodegeneration or cerebrovascular injury.
논문정보
- Research article
- 2020년 02월 (BRIC 등록일 2020-03-10)
- 국내 연구진
- 의약학 > 응용의학
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