title: Regional cortical thinning in subjects with high genetic loading for schizophrenia.
abstract: OBJECTIVE
  Although recent studies have revealed regional cortical thinning in patients with schizophrenia, it is not clear whether cortical thinning reflects a genetic liability for schizophrenia. The present study investigated the change of cortical thickness in subjects at genetic high risk (GHR) for schizophrenia with a relatively high genetic loading compared with healthy controls (HC) and patients with schizophrenia. The effect of genetic loading on cortical thinning was also measured by comparing GHR subgroups according to the levels of genetic loading.
  
  
  METHODS
  Cortical thickness was measured by the Constrained Laplacian-based Automated Segmentation with Proximities algorithm using 1.5-T structural MRI scans. The cortical thickness of the subjects at GHR (n=31) was compared with that of HC (n=29) and patients with schizophrenia (n=31). We then compared the cortical thickness of the GHR subgroups according to the number of first-degree relatives with schizophrenia to measure the effect of genetic loading.
  
  
  RESULTS
  Relative to HC, GHR subjects showed significant cortical thinning in the right anterior cingulate cortex (ACC), left paracingulate and posterior cingulate regions; bilateral frontal regions including frontal pole and ventromedial prefrontal cortex; bilateral temporal regions including the left parahippocampal gyrus; and bilateral inferior parietal and occipital regions; however, patients with schizophrenia showed more widespread cortical thinning in the fronto-temporo-parietal region. GHR subjects who had two or more first-degree relatives with schizophrenia showed a greater reduction in cortical thickness in the right ACC and in the left paracingulate cortex than did those who had only one first-degree relative with schizophrenia.
  
  
  CONCLUSIONS
  Our findings suggest that the level of genetic loading may have a dose-dependent effect on cortical thinning in the right ACC and in the left paracingulate cortex and that cortical thinning in GHR subjects may represent neurodevelopmental alterations that result from genetic liability for schizophrenia.
authors.affiliation: Department of Psychiatry, Seoul National University College of Medicine, Seoul, Republic of Korea. andyt@unimelb.edu.au
authors.forename: Min Soo
authors.initials: MS
authors.lastname: Byun
authors.forename: June Sic
authors.initials: JS
authors.lastname: Kim
authors.forename: Wi Hoon
authors.initials: WH
authors.lastname: Jung
authors.forename: Joon Hwan
authors.initials: JH
authors.lastname: Jang
authors.forename: Jung-Seok
authors.initials: JS
authors.lastname: Choi
authors.forename: Sung Nyun
authors.initials: SN
authors.lastname: Kim
authors.forename: Chi-Hoon
authors.initials: CH
authors.lastname: Choi
authors.forename: Chun Kee
authors.initials: CK
authors.lastname: Chung
authors.forename: Suk Kyoon
authors.initials: SK
authors.lastname: An
authors.forename: Jun Soo
authors.initials: JS
authors.lastname: Kwon
mesh_terms: D000293:Adolescent; D000328:Adult; D000704:Analysis of Variance; D001931:Brain Mapping; D016022:Case-Control Studies; D002540:Cerebral Cortex / Q000473:pathology*; D016009:Chi-Square Distribution; D005260:Female; D006801:Humans; D007091:Image Processing, Computer-Assisted; D008279:Magnetic Resonance Imaging; D008297:Male; D011569:Psychiatric Status Rating Scales; D012559:Schizophrenia / Q000235:genetics* / Q000473:pathology*; D055815:Young Adult