PMID- 25034946
OWN - NLM
STAT- MEDLINE
DCOM- 20150812
LR  - 20211021
IS  - 1873-2402 (Electronic)
IS  - 0006-3223 (Print)
IS  - 0006-3223 (Linking)
VI  - 77
IP  - 2
DP  - 2015 Jan 15
TI  - Progressive reduction in cortical thickness as psychosis develops: a multisite 
      longitudinal neuroimaging study of youth at elevated clinical risk.
PG  - 147-57
LID - S0006-3223(14)00414-4 [pii]
LID - 10.1016/j.biopsych.2014.05.023 [doi]
AB  - BACKGROUND: Individuals at clinical high risk (CHR) who progress to fully 
      psychotic symptoms have been observed to show a steeper rate of cortical gray 
      matter reduction compared with individuals without symptomatic progression and 
      with healthy control subjects. Whether such changes reflect processes associated 
      with the pathophysiology of schizophrenia or exposure to antipsychotic drugs is 
      unknown. METHODS: In this multisite study, 274 CHR cases, including 35 
      individuals who converted to psychosis, and 135 healthy comparison subjects were 
      scanned with magnetic resonance imaging at baseline, 12-month follow-up, or the 
      point of conversion for the subjects who developed fully psychotic symptoms. 
      RESULTS: In a traveling subjects substudy, excellent reliability was observed for 
      measures of cortical thickness and subcortical volumes. Controlling for multiple 
      comparisons throughout the brain, CHR subjects who converted to psychosis showed 
      a steeper rate of gray matter loss in the right superior frontal, middle frontal, 
      and medial orbitofrontal cortical regions as well as a greater rate of expansion 
      of the third ventricle compared with CHR subjects who did not convert to 
      psychosis and healthy control subjects. Differential tissue loss was present in 
      subjects who had not received antipsychotic medications during the interscan 
      interval and was predicted by baseline levels of an aggregate measure of 
      proinflammatory cytokines in plasma. CONCLUSIONS: These findings demonstrate that 
      the brain changes are not explained by exposure to antipsychotic drugs but likely 
      play a role in psychosis pathophysiology. Given that the cortical changes were 
      more pronounced in subjects with briefer durations of prodromal symptoms, 
      contributing factors may predominantly play a role in acute-onset forms of 
      psychosis.
CI  - Copyright (c) 2015 Society of Biological Psychiatry. All rights reserved.
FAU - Cannon, Tyrone D
AU  - Cannon TD
AD  - Departments of Psychology, Yale University, New Haven, Connecticut; Departments 
      of Psychiatry, Yale University, New Haven, Connecticut. Electronic address: 
      tyrone.cannon@yale.edu.
FAU - Chung, Yoonho
AU  - Chung Y
AD  - Departments of Psychology, Yale University, New Haven, Connecticut.
FAU - He, George
AU  - He G
AD  - Departments of Psychology, Yale University, New Haven, Connecticut.
FAU - Sun, Daqiang
AU  - Sun D
AD  - Semel Institute for Neuroscience and Human Behavior and Department of Psychology, 
      University of California, Los Angeles, Los Angeles, California.
FAU - Jacobson, Aron
AU  - Jacobson A
AD  - Departments of Psychology, Yale University, New Haven, Connecticut.
FAU - van Erp, Theo G M
AU  - van Erp TG
AD  - Department of Psychiatry, University of California, Irvine, Irvine, California.
FAU - McEwen, Sarah
AU  - McEwen S
AD  - Semel Institute for Neuroscience and Human Behavior and Department of Psychology, 
      University of California, Los Angeles, Los Angeles, California.
FAU - Addington, Jean
AU  - Addington J
AD  - Department of Psychiatry (JA), University of Calgary, Calgary, Alberta, Canada.
FAU - Bearden, Carrie E
AU  - Bearden CE
AD  - Semel Institute for Neuroscience and Human Behavior and Department of Psychology, 
      University of California, Los Angeles, Los Angeles, California.
FAU - Cadenhead, Kristin
AU  - Cadenhead K
AD  - Department of Psychiatry, University of California, San Diego, San Diego, 
      California.
FAU - Cornblatt, Barbara
AU  - Cornblatt B
AD  - Department of Psychiatry, Zucker Hillside Hospital, Glen Oaks, New York.
FAU - Mathalon, Daniel H
AU  - Mathalon DH
AD  - Department of Psychiatry, University of California, San Francisco, San Francisco, 
      California.
FAU - McGlashan, Thomas
AU  - McGlashan T
AD  - Departments of Psychiatry, Yale University, New Haven, Connecticut.
FAU - Perkins, Diana
AU  - Perkins D
AD  - Department of Psychiatry, University of North Carolina at Chapel Hill, Chapel 
      Hill, North Carolina.
FAU - Jeffries, Clark
AU  - Jeffries C
AD  - Renaissance Computing Institute, University of North Carolina at Chapel Hill, 
      Chapel Hill, North Carolina.
FAU - Seidman, Larry J
AU  - Seidman LJ
AD  - Department of Psychiatry, Beth Israel Deaconess Medical Center and Massachusetts 
      General Hospital, Harvard Medical School, Boston, Massachusetts.
FAU - Tsuang, Ming
AU  - Tsuang M
AD  - Department of Psychiatry, University of California, San Diego, San Diego, 
      California.
FAU - Walker, Elaine
AU  - Walker E
AD  - Department of Psychology, Emory University, Atlanta, Georgia.
FAU - Woods, Scott W
AU  - Woods SW
AD  - Departments of Psychiatry, Yale University, New Haven, Connecticut.
FAU - Heinssen, Robert
AU  - Heinssen R
AD  - Division of Treatment and Prevention Research, National Institute of Mental 
      Health, Rockville, Maryland.
CN  - North American Prodrome Longitudinal Study Consortium
LA  - eng
GR  - MH081902/MH/NIMH NIH HHS/United States
GR  - MH081928/MH/NIMH NIH HHS/United States
GR  - P50 MH080272/MH/NIMH NIH HHS/United States
GR  - MH081984/MH/NIMH NIH HHS/United States
GR  - U01 MH081988/MH/NIMH NIH HHS/United States
GR  - U54 EB020403/EB/NIBIB NIH HHS/United States
GR  - P50 MH066286/MH/NIMH NIH HHS/United States
GR  - MH082022/MH/NIMH NIH HHS/United States
GR  - U01 MH066160/MH/NIMH NIH HHS/United States
GR  - MH081857/MH/NIMH NIH HHS/United States
GR  - U01 MH081928/MH/NIMH NIH HHS/United States
GR  - MH066160/MH/NIMH NIH HHS/United States
GR  - P30 ES010126/ES/NIEHS NIH HHS/United States
GR  - U01 MH082022/MH/NIMH NIH HHS/United States
GR  - U01 MH081984/MH/NIMH NIH HHS/United States
GR  - MH081988/MH/NIMH NIH HHS/United States
GR  - U01 MH081902/MH/NIMH NIH HHS/United States
GR  - U01 MH076989/MH/NIMH NIH HHS/United States
GR  - MH082004/MH/NIMH NIH HHS/United States
GR  - U01 MH081857/MH/NIMH NIH HHS/United States
GR  - U01 MH082004/MH/NIMH NIH HHS/United States
GR  - U01 MH081944/MH/NIMH NIH HHS/United States
PT  - Journal Article
PT  - Multicenter Study
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20140612
PL  - United States
TA  - Biol Psychiatry
JT  - Biological psychiatry
JID - 0213264
RN  - 0 (Antipsychotic Agents)
RN  - 0 (Cytokines)
SB  - IM
MH  - Adolescent
MH  - Antipsychotic Agents/therapeutic use
MH  - Cerebral Cortex/drug effects/*pathology
MH  - Cytokines/blood
MH  - Disease Progression
MH  - Female
MH  - Follow-Up Studies
MH  - Humans
MH  - Longitudinal Studies
MH  - Magnetic Resonance Imaging
MH  - Male
MH  - Organ Size
MH  - Prodromal Symptoms
MH  - Psychotic Disorders/blood/drug therapy/*pathology
MH  - Reproducibility of Results
MH  - Risk
MH  - Young Adult
PMC - PMC4264996
MID - NIHMS614962
OTO - NOTNLM
OT  - Inflammation
OT  - MRI
OT  - Prefrontal cortex
OT  - Prodromal
OT  - Psychosis
OT  - Schizophrenia
COIS- Conflict of Interest All authors report no biomedical financial interests or 
      potential conflicts of interest.
EDAT- 2014/07/19 06:00
MHDA- 2015/08/13 06:00
PMCR- 2016/01/15
CRDT- 2014/07/19 06:00
PHST- 2014/03/06 00:00 [received]
PHST- 2014/05/17 00:00 [revised]
PHST- 2014/05/25 00:00 [accepted]
PHST- 2014/07/19 06:00 [entrez]
PHST- 2014/07/19 06:00 [pubmed]
PHST- 2015/08/13 06:00 [medline]
PHST- 2016/01/15 00:00 [pmc-release]
AID - S0006-3223(14)00414-4 [pii]
AID - 10.1016/j.biopsych.2014.05.023 [doi]
PST - ppublish
SO  - Biol Psychiatry. 2015 Jan 15;77(2):147-57. doi: 10.1016/j.biopsych.2014.05.023. 
      Epub 2014 Jun 12.