Hippocampal subfield CA2+3 exhibits accelerated aging in Alcohol Use Disorder: A preliminary study
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Affiliation
Univ Arizona, Coll Med, Dept Med ImagingIssue Date
2019Keywords
Alcohol Use Disorder (AUD)Attention
Executive functions
Hippocampal subfields
Hippocampal subregions
Hippocampus
Learning and memory
Visuospatial
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ELSEVIER SCI LTDCitation
Zahr, N. M., Pohl, K. M., Saranathan, M., Sullivan, E. V., & Pfefferbaum, A. (2019). Hippocampal subfield CA2+ 3 exhibits accelerated aging in Alcohol Use Disorder: A preliminary study. NeuroImage: Clinical, 22, 101764.Journal
NEUROIMAGE-CLINICALRights
© 2019 The Author(s). Published by Elsevier Inc. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/BY-NC-ND/4.0/).Collection Information
This item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at repository@u.library.arizona.edu.Abstract
The profile of brain structural dysmorphology of individuals with Alcohol Use Disorders (AUD) involves disruption of the limbic system. In vivo imaging studies report hippocampal volume loss in AUD relative to controls, but only recently has it been possible to articulate different regions of this complex structure. Volumetric analysis of hippocampal regions rather than total hippocampal volume may augment differentiation of disease processes. For example, damage to hippocampal subfield cornu ammonis 1 (CA1) is often reported in Alzheimer's disease (AD), whereas deficits in CA4/dentate gyrus are described in response to stress and trauma. Two previous studies explored the effects of chronic alcohol use on hippocampal subfields: one reported smaller volume of the CA2 + 3 in alcohol-dependent subjects relative to controls, associated with years of alcohol consumption; the other, smaller volumes of presubiculum, subiculum, and fimbria in alcohol-dependent relative to control men. The current study, conducted in 24 adults with DSM5-diagnosed AUD (7 women, 53.7 +/- 8.8) and 20 controls (7 women, 54.1 +/- 9.3), is the first to use FreeSurfer 6.0, which provides state-of-the art hippocampal parcellation, to explore the sensitivity of hippocampal sufields to alcoholism. T1- and T2- images were collected on a GE MR750 system with a 32-channel Nova head coil. FreeSurfer 6.0 hippocampal subfield analysis produced 12 subfields: parasubiculum; presubiculum; subiculum; CAl; CA2 + 3; CA4; GC-ML-DG (Granule Cell (GC) and Molecular Layer (ML) of the Dentate Gyrus (DG)); molecular layer; hippocampus-amygdala-transition-area (HATA); fimbria; hippocampal tail; hippocampal fissure; and whole volume for left and right hippocampi. A comprehensive battery of neuropsychological tests comprising attention, memory and learning, visuospatial abilities, and executive functions was administered. Multiple regression analyses of raw volumetric data for each subfields by group, age, sex, hemisphere, and supratentorial volume (svol) showed significant effects of svol (p < .04) on nearly all structures (excluding tail and fissure). Volumes corrected for svol showed effects of age (fimbria, fissure) and group (subiculum, CA1, CA4, GC-ML-DG, HATA, fimbria); CA2 + 3 showed a diagnosis-by-age interaction indicating older AUD individuals had a smaller volume than would be expected for their age. There were no selective relations between hippocampal subfields and performance on neuropsychological tests, likely due to lack of statistical power. The current results concur with the previous study identifying CA2 + 3 as sensitive to alcoholism, extend them by identifying an alcoholism-age interaction, and suggest an imaging phenotype distinguishing AUD from AD and stress/trauma.Note
Open access journalISSN
2213-1582PubMed ID
30904825Version
Final published versionSponsors
National Institute of Alcohol Abuse and Alcoholism [R21 AA023582, R01 AA005965, R37 AA010723, U01 AA013521]; National Institute of Mental Health [R01 MH113406]ae974a485f413a2113503eed53cd6c53
10.1016/j.nicl.2019.101764
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Except where otherwise noted, this item's license is described as © 2019 The Author(s). Published by Elsevier Inc. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/BY-NC-ND/4.0/).
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