Cigarette smoking exacerbates chronic alcohol-induced brain damage: A preliminary metabolite imaging study
Cigarette smoking exacerbates chronic alcohol-induced brain damage: A preliminary metabolite imaging study
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DOI：
10.1097/01.alc.0000148112.92525.ac
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发表时间：
2004-12-01
期刊：
影响因子：
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通讯作者：
Meyerhoff, DJ
中科院分区：
文献类型：
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作者：
Durazzo, TC;Gazdzinski, S;Meyerhoff, DJ
背景：吸烟在酒精依赖者中很常见。然而，以往的研究通常没有考虑到吸烟对酒精诱导的脑损伤和神经认知的潜在独立或复合影响。（RA; 14名吸烟者和10名非吸烟者）和26名轻度饮酒对照比较了7名吸烟者和19名非吸烟者在大脑主要脑叶、基底节、中脑和小脑蚓部的灰质和白色物质中常见脑代谢物的测量结果，通过多层短回波时间质子磁共振光谱成像获得。吸烟和不吸烟的RA的神经认知功能的措施，以及饮酒的严重程度和营养状况的实验室标志物进行了对比。结果：慢性酒精依赖，独立于吸烟，与较低浓度的额叶N-乙酰天门冬氨酸（NAA）和额叶含胆碱的化合物，以及较低的顶叶和丘脑胆碱。吸烟的RA有较低的NAA浓度在额叶白色物质和中脑和较低的中脑胆碱比不吸烟的RA。四组协方差分析也表明，慢性吸烟与较低的中脑NAA和胆碱，并与较低的蠕虫胆碱。在吸烟的RA中，酗酒与吸烟有关，这与许多皮质下代谢物异常有关。戒烟1周和不吸烟的RA在简短的神经认知电池上没有显着差异。在吸烟的RA中，小脑蚓部NAA与较差的视觉扫描速度和偶然学习有关，而在非吸烟的RA中，小脑蚓部NAA与较差的视觉空间学习和记忆有关。这些人体体内质子磁共振光谱成像结果表明，慢性吸烟加剧了慢性酒精中毒，在RA的额叶中诱导神经元损伤和细胞膜损伤，并且对中脑中的神经元活力和细胞膜以及小脑蚓部的细胞膜具有独立的不利影响。较高的吸烟水平与某些皮质下结构中的代谢物浓度有关。更多地考虑吸烟对酒精引起的脑损伤和其他影响中枢神经系统的疾病的潜在影响是必要的。
Background: Cigarette smoking is common among alcohol-dependent individuals. Nevertheless, previous research has typically not accounted for the potential independent or compounding effects of cigarette smoking on alcohol-induced brain injury and neurocognition.Methods: Twenty-four 1-week-abstinent recovering alcoholics (RAs; 14 smokers and 10 nonsmokers) in treatment and 26 light-drinking controls (7 smokers and 19 nonsmokers) were compared on measures of common brain metabolites in gray matter and white matter of the major lobes, basal ganglia, midbrain, and cerebellar vermis, obtained via multislice short-echo time proton magnetic resonance spectroscopic imaging. Smoking and nonsmoking RAs were also contrasted on measures of neurocognitive functioning, as well as laboratory markers of drinking severity and nutritional status.Results: Chronic alcohol dependence, independent of smoking, was associated with lower concentrations of frontal N-acetylaspartate (NAA) and frontal choline-containing compounds, as well as lower parietal and thalamic choline. Smoking RAs had lower NAA concentrations in frontal white matter and midbrain and lower midbrain choline than nonsmoking RAs. A four-group analysis of covariance also demonstrated that chronic cigarette smoking was associated with lower midbrain NAA and choline and with lower vermian choline. In smoking RAs, heavier drinking was associated with heavier smoking, which correlated with numerous subcortical metabolite abnormalities. The 1-week-abstinent smoking and nonsmoking RAs did not differ significantly on a brief neurocognitive battery. In smoking RAs, lower cerebellar vermis NAA was associated with poorer visuomotor scanning speed and incidental learning, and in nonsmoking RAs lower vermis NAA was related to poorer visuospatial learning and memory.Conclusions: These human in vivo proton magnetic resonance spectroscopic imaging findings indicate that chronic cigarette smoking exacerbates chronic alcohol-induced neuronal injury and cell membrane damage in the frontal lobes of RAs and has independent adverse effects on neuronal viability and cell membranes in the midbrain and on cell membranes of the cerebellar vermis. Higher smoking levels are associated with metabolite concentrations in select subcortical structures. Greater consideration of the potential effects of comorbid cigarette smoking on alcohol-induced brain damage and other diseases affecting the central nervous system is warranted.