Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, 401 Quarry Rd., Stanford, CA 94305, USA; Mental Illness Research and Education Clinical Centers and Sierra-Pacific, War Related Illness and Injury Study Center, VA Palo Alto Health Care System, 301 Miranda Ave., Palo Alto, CA 94304, USA.
Department of Radiology and Biomedical Imaging, University of California, San Francisco, 505 Parnassus Ave, San Francisco, CA 94143, USA; Center for Imaging of Neurodegenerative Diseases, San Francisco VA Medical Center, 4150 Clement St., 114M, San Francisco, CA 94121, USA.
Drug Alcohol Depend. 2018 Nov 1;192:277-284. doi: 10.1016/j.drugalcdep.2018.08.009. Epub 2018 Sep 29.
Magnetic resonance imaging studies of cigarette smoking-related effects on human brain structure primarily focused on cortical volumes. Much less is known about the effects of smoking on cortical thickness. Smokers and Non-smokers were compared on regional cortical thickness. We predicted smokers would demonstrate greater age-related thinning localized to anterior frontal regions that serve as nodes for the executive, salience, and emotional regulation networks (ESER regions) and those demonstrating significant atrophy in early Alzheimer's Disease (AD regions).
Non-smokers (n = 41) and smokers (n = 41), 22-70 years of age, completed a 4 T MRI study. Regional cortical thickness was quantitated via FreeSurfer. In smokers, associations between smoking severity, decision-making, impulsivity, and regional cortical thickness were examined.
Smokers demonstrated cortical thinning in the medial and lateral OFC, insula, entorhinal, fusiform, middle temporal, and Composite AD regions. In Smokers, greater pack-years were associated with thinner lateral OFC, middle temporal, inferior parietal, fusiform, precuneus, and Composite AD regions. In Smokers, poorer decision-making/greater risk taking was related to thinner cortices in caudal ACC, rostral middle frontal and superior frontal gyri, and Composite ESER. Higher self-reported impulsivity was associated with thinner rostral and caudal ACC.
This study provides additional evidence that cigarette smoking is associated with thinner cortices in regions implicated in the development and maintenance of substance use disorders and in regions demonstrating significant atrophy in early AD. The novel structure-function relationships in Smokers further our understanding of the neurobiological substrates potentially underlying the neuropsychological abnormalities documented in smokers.
磁共振成像研究表明,吸烟与人类大脑结构的变化主要与皮质体积有关。而关于吸烟对皮质厚度影响的研究则知之甚少。本研究比较了吸烟者和非吸烟者的皮质厚度。我们预测吸烟者会表现出与年龄相关的皮质变薄,这种变薄主要局限于额前区域,这些区域是执行、突显和情绪调节网络(ESER 区域)的节点,以及那些在早期阿尔茨海默病(AD 区域)中表现出明显萎缩的区域。
非吸烟者(n=41)和吸烟者(n=41)年龄在 22-70 岁之间,完成了 4T MRI 研究。通过 FreeSurfer 定量分析皮质厚度。在吸烟者中,还检查了吸烟严重程度、决策、冲动与皮质厚度之间的关系。
吸烟者表现出内侧和外侧眶额皮质、岛叶、内嗅皮质、梭状回、颞中回和综合 AD 区域的皮质变薄。在吸烟者中,吸烟年限与外侧眶额皮质、颞中回、下顶叶、梭状回、楔前叶和综合 AD 区域的皮质变薄有关。在吸烟者中,较差的决策/更高的冒险行为与后扣带回皮质、额中回和额上回的皮质变薄有关。较高的自我报告冲动与前后扣带回皮质变薄有关。
本研究进一步证明,吸烟与物质使用障碍发展和维持相关的区域以及在早期 AD 中表现出明显萎缩的区域的皮质变薄有关。吸烟者中存在新的结构-功能关系,进一步加深了我们对潜在神经生物学基础的理解,这些基础可能是吸烟者神经心理学异常的基础。