Comorbid HIV infection and alcohol use disorders: Converging glutamatergic and dopaminergic mechanisms underlying neurocognitive dysfunction.
Comorbid HIV infection and alcohol use disorders: Converging glutamatergic and dopaminergic mechanisms underlying neurocognitive dysfunction.
复制标题
共病艾滋病毒感染和酒精使用障碍：神经认知功能障碍的谷氨酸能和多巴胺能机制的融合。
DOI：
10.1016/j.brainres.2019.146390
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发表时间：
2019
期刊：
影响因子：
2.9
通讯作者：
Barker,JacquelineM
中科院分区：
文献类型：
--
作者：
Giacometti,LauraL;Barker,JacquelineM
酒精使用障碍(AUD)与人类免疫缺陷病毒(HIV)感染高度共存，艾滋病毒阳性个人的发病率几乎是普通人群的两倍。饮酒的艾滋病毒携带者长期预后更差，患艾滋病毒相关神经认知障碍的风险可能更高。这种关系的方向尚不清楚，可能是多因素的。慢性酒精暴露和艾滋病毒感染独立地促进认知功能障碍，并进一步可能通过对共同靶点的影响而相互作用，加剧神经认知障碍，包括皮质纹状体谷氨酸和多巴胺神经传递。此外，药物和酒精的使用可能会降低治疗的依从性，可能导致疾病加速发展和随后的神经认知障碍。神经认知障碍的发展可能会进一步降低对行为的认知控制，导致酒精使用的升级。这篇综述将研究HIV感染和酒精使用之间的复杂关系，重点是对多巴胺和谷氨酸系统的影响，酒精使用和HIV通过这些系统独立地和联合地作用于改变皮质纹状体回路结构和功能，从而调节认知功能。
Alcohol use disorders (AUDs) are highly comorbid with human immunodeficiency virus (HIV) infection, occurring at nearly twice the rate in HIV positive individuals as in the general population. Individuals with HIV who consume alcohol show worse long-term prognoses and may be at elevated risk for the development of HIV-associated neurocognitive disorders. The direction of this relationship is unclear, and likely multifactorial. Chronic alcohol exposure and HIV infection independently promote cognitive dysfunction and further may interact to exacerbate neurocognitive deficits through effects on common targets, including corticostriatal glutamate and dopamine neurotransmission. Additionally, drug and alcohol use is likely to reduce treatment adherence, potentially resulting in accelerated disease progression and subsequent neurocognitive impairment. The development of neurocognitive impairments may further reduce cognitive control over behavior, resulting in escalating alcohol use. This review will examine the complex relationship between HIV infection and alcohol use, highlighting impacts on dopamine and glutamate systems by which alcohol use and HIV act independently and in tandem to alter corticostriatal circuit structure and function to dysregulate cognitive function.