Frontal Brain N-Acetylaspartate at Treatment Entry is Related to Future WHO Risk Drinking Levels in Individuals with Alcohol Use Disorder.

IF 2.4 3区 医学 Q2 PSYCHOLOGY Journal of studies on alcohol and drugs Pub Date : 2024-08-10 DOI:10.15288/jsad.24-00168
April C May, Lauren H Stephens, Eric P Kraybill, Dieter J Meyerhoff, Timothy C Durazzo
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Abstract

Objective: To assess the viability of regional brain metabolite levels of individuals with alcohol use disorder (AUD) at treatment entry as a biomarker of post-treatment levels of alcohol use, categorized according to the World Health Organization risk drinking levels (WHO-RDL).

Method: Eighty-five individuals initiating treatment for AUD (16 ± 13 days after last alcohol consumption), and 45 light/non-drinking controls (LN) completed a 1.5T proton multislice magnetic resonance spectroscopic imaging study. N-acetylaspartate (NAA), a marker of neuronal viability, and other metabolites were quantitated for cortical gray matter (GM), white matter (WM) and select subcortical regions. Individuals with AUD were classified according to their post-treatment alcohol consumption, as abstainers (AB, n=42), low risk (RL, n=20), or higher risk (RH, n=23), based on the WHO-RDL taxonomy.

Results: Within frontal GM, RH exhibited significantly lower NAA levels than LN and AB but did not differ from RL. RH had significantly lower NAA concentration in frontal WM than all groups who did not significantly differ from one another. RH showed significantly lower parietal WM NAA than LN and AB; RL and RH did not differ from one another. Across RH and RL, lower frontal GM and WM NAA was related to shorter period of abstinence before first post-treatment alcohol consumption and longer post-treatment duration of alcohol resumption. There were no significant group differences in myo-inositol or choline- or creatine-containing compound concentrations.

Conclusions: Frontal and parietal lobar NAA concentrations, near treatment entry, are associated with WHO-RDL categorized post-treatment alcohol consumption levels and may serve as predictive biomarkers of clinical outcomes following treatment for AUD.

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开始治疗时的大脑额叶 N-乙酰天冬氨酸与酒精使用障碍患者未来的世界卫生组织风险饮酒水平有关。
目的评估根据世界卫生组织危险饮酒水平(WHO-RDL)分类的酒精使用障碍(AUD)患者在开始治疗时大脑区域代谢物水平作为治疗后酒精使用水平生物标志物的可行性:方法:85 名开始接受 AUD 治疗的人(最后一次饮酒后 16 ± 13 天)和 45 名轻度/不饮酒对照者(LN)完成了一项 1.5T 质子多层磁共振光谱成像研究。研究人员对皮质灰质(GM)、白质(WM)和部分皮质下区域的神经元活力标志物--N-乙酰天冬氨酸(NAA)及其他代谢物进行了定量分析。根据WHO-RDL分类法,根据治疗后的饮酒量将AUD患者分为戒酒者(AB,42人)、低风险者(RL,20人)或高风险者(RH,23人):在额叶基因组中,RH的NAA水平明显低于LN和AB,但与RL没有差异。在额叶WM中,RH的NAA浓度明显低于所有组别,但各组之间无明显差异。RH的顶叶WM NAA含量明显低于LN和AB,而RL和RH则无明显差异。在RH和RL中,额叶GM和WM NAA较低与治疗后首次饮酒前的戒酒时间较短和治疗后恢复饮酒的时间较长有关。肌醇、胆碱或含肌酸化合物的浓度没有明显的组间差异:额叶和顶叶的NAA浓度在治疗开始时与WHO-RDL分类的治疗后饮酒水平相关,可作为AUD治疗后临床结果的预测性生物标志物。
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来源期刊
CiteScore
4.80
自引率
5.90%
发文量
224
审稿时长
3 months
期刊介绍: The Journal of Studies on Alcohol and Drugs began in 1940 as the Quarterly Journal of Studies on Alcohol. It was founded by Howard W. Haggard, M.D., director of Yale University’s Laboratory of Applied Physiology. Dr. Haggard was a physiologist studying the effects of alcohol on the body, and he started the Journal as a way to publish the increasing amount of research on alcohol use, abuse, and treatment that emerged from Yale and other institutions in the years following the repeal of Prohibition in 1933. In addition to original research, the Journal also published abstracts summarizing other published documents dealing with alcohol. At Yale, Dr. Haggard built a large team of alcohol researchers within the Laboratory of Applied Physiology—including E.M. Jellinek, who became managing editor of the Journal in 1941. In 1943, to bring together the various alcohol research projects conducted by the Laboratory, Dr. Haggard formed the Section of Studies on Alcohol, which also became home to the Journal and its editorial staff. In 1950, the Section was renamed the Center of Alcohol Studies.
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