与酒精使用障碍家族史相关的神经相关性:最新研究成果综述。

IF 3 Q2 SUBSTANCE ABUSE Alcohol (Hanover, York County, Pa.) Pub Date : 2024-11-17 DOI:10.1111/acer.15488
Anita Cservenka, Sheeva Azma
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引用次数: 0

摘要

有酒精使用障碍(AUD)家族史的人一生中患酒精使用障碍的风险会显著增加。之前的文献综述表明,有一些结构性和功能性神经生物学标志物与家族性 AUD 有关,但据我们所知,近期还没有综述对这一高危人群的神经影像学研究的最新发现进行归纳。在这篇叙述性综述中,我们在电子数据库中进行了关键词搜索,以找到使用磁共振成像(MRI)、弥散张量成像、任务型功能磁共振成像(fMRI)和/或静息状态功能连接磁共振成像的横断面和纵向研究(2015 年至今)。这些研究用于识别有 AUD 家族史的家族史阳性 (FHP) 患者的灰质、白质和大脑活动标志物。与无家族性 AUD 的家族性阴性 (FHN) 同龄人相比,FHP 患者的执行功能(额叶)区域在青春期早期更薄弱;然而,一些研究报告称,与无家族性 AUD 的家族性阴性 (FHN) 同龄人相比,FHP 患者的灰质体积和厚度无影响或更大。FHP 患者的白质微结构也会发生改变,如前额纹状体通路的完整性降低。最近的 fMRI 研究发现,FHP 患者的抑制控制活动更强,而与奖赏相关的研究结果则不尽相同。近年来,人们对识别 FHP 和 FHN 患者之间内在连通性差异的兴趣日益浓厚。家族性 AUD 与大脑结构和功能的改变都有关系。研究应继续关注:(1)更大样本的纵向分析;(2)对个人药物使用和产前酒精暴露的评估;(3)合并家族性精神病理学的影响;(4)风险和恢复力的性别特异性标记;(5)酒精使用起始的神经预测因素;(6)大脑与行为的关系。这些工作将有助于设计针对这一高危人群的神经生物学预防和干预措施。
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Neural correlates associated with a family history of alcohol use disorder: A narrative review of recent findings.

A family history of alcohol use disorder (AUD) is associated with a significantly increased risk of developing AUD in one's lifetime. The previously reviewed literature suggests there are structural and functional neurobiological markers associated with familial AUD, but to our knowledge, no recent review has synthesized the latest findings across neuroimaging studies in this at-risk population. For this narrative review, we conducted keyword searches in electronic databases to find cross-sectional and longitudinal studies (2015-present) that used magnetic resonance imaging (MRI), diffusion tensor imaging, task-based functional MRI (fMRI), and/or resting state functional connectivity MRI. These studies were used to identify gray matter, white matter, and brain activity markers of risk and resilience in family history positive (FHP) individuals with a family history of AUD. FHP individuals have greater early adolescent thinning of executive functioning (frontal lobe) regions; however, some studies have reported null effects or greater gray matter volume and thickness relative to family history negative (FHN) peers without familial AUD. FHP individuals also have white matter microstructure alterations, such as reduced integrity of fronto-striatal pathways. Recent fMRI studies have found greater inhibitory control activity in FHP individuals, while reward-related findings are mixed. A growing interest in identifying intrinsic connectivity differences between FHP and FHN individuals has emerged in recent years. Familial AUD is related to both structural and functional brain alterations. Research should continue to focus on (1) longitudinal analyses with larger samples, (2) assessment of personal substance use and prenatal exposure to alcohol, (3) the effects of comorbid familial psychopathology, (4) examination of sex-specific markers of risk and resilience, (5) neural predictors of alcohol use initiation, and (6) brain-behavior relationships. These efforts would aid the design of neurobiologically informed prevention and intervention efforts focused on this at-risk population.

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