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      Abnormal White Matter Integrity in the Corpus Callosum among Smokers: Tract-Based Spatial Statistics

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          Abstract

          In the present study, we aimed to investigate the difference in white matter between smokers and nonsmokers. In addition, we examined relationships between white matter integrity and nicotine dependence parameters in smoking subjects. Nineteen male smokers were enrolled in this study. Eighteen age-matched non-smokers with no current or past psychiatric history were included as controls. Diffusion tensor imaging scans were performed, and the analysis was conducted using a tract-based special statistics approach. Compared with nonsmokers, smokers exhibited a significant decrease in fractional anisotropy (FA) throughout the whole corpus callosum. There were no significant differences in radial diffusivity or axial diffusivity between the two groups. There was a significant negative correlation between FA in the whole corpus callosum and the amount of tobacco use (cigarettes/day; R = − 0.580, p = 0.023). These results suggest that the corpus callosum may be one of the key areas influenced by chronic smoking.

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          Most cited references25

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          Demyelination increases radial diffusivity in corpus callosum of mouse brain.

          Myelin damage, as seen in multiple sclerosis (MS) and other demyelinating diseases, impairs axonal conduction and can also be associated with axonal degeneration. Accurate assessments of these conditions may be highly beneficial in evaluating and selecting therapeutic strategies for patient management. Recently, an analytical approach examining diffusion tensor imaging (DTI) derived parameters has been proposed to assess the extent of axonal damage, demyelination, or both. The current study uses the well-characterized cuprizone model of experimental demyelination and remyelination of corpus callosum in mouse brain to evaluate the ability of DTI parameters to detect the progression of myelin degeneration and regeneration. Our results demonstrate that the extent of increased radial diffusivity reflects the severity of demyelination in corpus callosum of mouse brain affected by cuprizone treatment. Subsequently, radial diffusivity decreases with the progression of remyelination. Furthermore, radial diffusivity changes were specific to the time course of changes in myelin integrity as distinct from axonal injury, which was detected by betaAPP immunostaining and shown to be most extensive prior to demyelination. Radial diffusivity offers a specific assessment of demyelination and remyelination, as distinct from acute axonal damage.
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            Computational anatomy with the SPM software.

            An overview of computational procedures for examining neuroanatomical variability is presented. The review focuses on approaches that can be applied using the SPM software package, beginning by explaining briefly how statistical parametric mapping is usually applied to functional imaging data. The review then proceeds to discuss volumetry, with an emphasis on voxel-based morphometry, and the pre-processing steps involved using the SPM software. Most volumetric studies involve univariate approaches, with a correction for some global measure, such as total brain volume. In contrast, the overall form of the brain may be more accurately modeled using multivariate approaches. Such models of anatomical variability may prove accurate enough for computer assisted diagnoses.
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              Noninvasive detection of cuprizone induced axonal damage and demyelination in the mouse corpus callosum.

              Previously, we tested the prediction that axonal damage results in decreased axial diffusivity (lambda(parallel)) while demyelination leads to increased radial diffusivity (lambda(perpendicular)). Cuprizone treatment of C57BL/6 mice was a highly reproducible model of CNS white matter demyelination and remyelination affecting the corpus callosum (CC). In the present study, six C57BL/6 male mice were fed 0.2% cuprizone for 12 weeks followed by 12 weeks of recovery on normal chow. The control mice were fed normal chow and imaged in parallel. Biweekly in vivo DTI examinations showed transient decrease of lambda(parallel) in CC at 2-6 weeks of cuprizone treatment. Immunostaining for nonphosphorylated neurofilaments demonstrated corresponding axonal damage at 4 weeks of treatment. Significant demyelination was evident from loss of Luxol fast blue staining at 6-12 weeks of cuprizone ingestion and was paralleled by increased lambda(perpendicular) values, followed by partial normalization during the remyelination phase. The sensitivity of lambda(perpendicular) to detect demyelination may be modulated in the presence of axonal damage during the early stage of demyelination at 4 weeks of cuprizone treatment. Our results suggest that lambda(parallel) and lambda(perpendicular) may be useful in vivo surrogate markers of axonal and myelin damage in mouse CNS white matter. Copyright 2006 Wiley-Liss, Inc.
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                Author and article information

                Contributors
                Role: Editor
                Journal
                PLoS One
                PLoS ONE
                plos
                plosone
                PLoS ONE
                Public Library of Science (San Francisco, USA )
                1932-6203
                2014
                7 February 2014
                : 9
                : 2
                : e87890
                Affiliations
                [1 ]Department of Psychiatry, University of Occupational and Environmental Health, Kitakyushu, Japan
                [2 ]Department of Radiology, University of Occupational and Environmental Health, Kitakyushu, Japan
                [3 ]Department of Psychiatry, Kyoto University Graduate School of Medicine, Kyoto, Japan
                [4 ]Department of Radiology, School of Medicine, Nihon University, Tokyo, Japan
                “Mario Negri” Institute for Pharmacological Research, Italy
                Author notes

                Competing Interests: The authors have the following interests: This study was supported by Dainippon Sumitomo Pharma Co. Ltd. and Otsuka Pharmaceutical Co. Ltd. There are no patents, products in development or marketed products to declare. This does not alter the authors’ adherence to all the PLOS ONE policies on sharing data and materials, as detailed online in the guide for authors.

                Conceived and designed the experiments: WU-N RY SK HT. Performed the experiments: WU-N SK KH HH AI-S AK KA J. Nishimura. Analyzed the data: WU-N SK KW. Contributed reagents/materials/analysis tools: WU-N RY SK KW KH JM SI IU. Wrote the paper: WU-N RY SK KW HT OA YK J. Nakamura.

                Article
                PONE-D-13-40074
                10.1371/journal.pone.0087890
                3917830
                be98f476-fac0-4dcb-aae3-353cf91bebfe
                Copyright @ 2014

                This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

                History
                : 30 September 2013
                : 5 January 2014
                Page count
                Pages: 6
                Funding
                Professor Jun Nakamura has received grant support from Dainippon Sumitomo Pharma Co. Ltd. and Otsuka Pharmaceutical Co. Ltd in 2012. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
                Categories
                Research Article
                Biology
                Population Biology
                Medicine
                Clinical Research Design
                Epidemiology
                Clinical Epidemiology
                Mental Health
                Psychology
                Clinical Psychology
                Pulmonology
                Smoking Related Disorders
                Radiology
                Social and Behavioral Sciences
                Psychology
                Clinical Psychology

                Uncategorized
                Uncategorized

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