Timothy C Durazzo1, Dieter J Meyerhoff2, Karmen K Yoder3. 1. 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. Electronic address: tdurazzo@stanford.edu. 2. 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. 3. Indiana University Center for Neuroimaging, Department of Radiology and Imaging Sciences, Indiana University School of Medicine, 550 N. University Blvd., Indianapolis, IN 46202, USA.
Abstract
BACKGROUND: 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). METHODS: 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. RESULTS: 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. CONCLUSIONS: 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. Published by Elsevier B.V.
BACKGROUND: 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). METHODS: 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. RESULTS: 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. CONCLUSIONS: 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. Published by Elsevier B.V.
Authors: Dardo G Tomasi; Corinde E Wiers; Ehsan Shokri-Kojori; Amna Zehra; Veronica Ramirez; Clara Freeman; Jamie Burns; Christopher Kure Liu; Peter Manza; Sung W Kim; Gene-Jack Wang; Nora D Volkow Journal: Int J Neuropsychopharmacol Date: 2019-09-01 Impact factor: 5.176
Authors: Nathan Whitsel; Chandra A Reynolds; Erik J Buchholz; Shandell Pahlen; Rahul C Pearce; Sean N Hatton; Jeremy A Elman; Nathan A Gillespie; Daniel E Gustavson; Olivia K Puckett; Anders M Dale; Lisa T Eyler; Christine Fennema-Notestine; Donald J Hagler; Richard L Hauger; Linda K McEvoy; Ruth McKenzie; Michael C Neale; Matthew S Panizzon; Mark Sanderson-Cimino; Rosemary Toomey; Xin M Tu; Mc Kenna E Williams; Tyler Bell; Hong Xian; Michael J Lyons; William S Kremen; Carol E Franz Journal: Addiction Date: 2021-10-28 Impact factor: 6.526