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      Cortical Brain Development in Schizophrenia: Insights From Neuroimaging Studies in Childhood-Onset Schizophrenia

      research-article
      Author(s): 1 , 2
      Publication date (Electronic):
      Journal: Schizophrenia Bulletin
      Publisher: Oxford University Press
      Keywords: childhood-onset schizophrenia, structural brain imaging

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          Abstract

          Childhood-onset schizophrenia (COS; defined as onset by age 12 years) is rare, difficult to diagnose, and represents a severe and chronic phenotype of the adult-onset illness. A study of childhood-onset psychoses has been ongoing at the National Institute of Mental Health (NIMH) since 1990, where children with COS and severe atypical psychoses (provisionally labeled “multidimensionally impaired” or MDI by the NIMH team) are studied prospectively along with all first-degree relatives. COS subjects have robust cortical gray matter (GM) loss during adolescence, which appears to be an exaggeration of the normal cortical GM developmental pattern and eventually mimics the pattern seen in adult-onset cases as the children become young adults. These cortical GM changes in COS are diagnostically specific and seemingly unrelated to the effects of medications. Furthermore, the cortical GM loss is also shared by healthy full siblings of COS probands suggesting a genetic influence on the abnormal brain development.

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          Regional differences in synaptogenesis in human cerebral cortex.

          P Huttenlocher, A S Dabholkar (1997)
          The formation of synaptic contacts in human cerebral cortex was compared in two cortical regions: auditory cortex (Heschl's gyrus) and prefrontal cortex (middle frontal gyrus). Synapse formation in both cortical regions begins in the fetus, before conceptual age 27 weeks. Synaptic density increases more rapidly in auditory cortex, where the maximum is reached near postnatal age 3 months. Maximum synaptic density in middle frontal gyrus is not reached until after age 15 months. Synaptogenesis occurs concurrently with dendritic and axonal growth and with myelination of the subcortical white matter. A phase of net synapse elimination occurs late in childhood, earlier in auditory cortex, where it has ended by age 12 years, than in prefrontal cortex, where it extends to midadolescence. Synaptogenesis and synapse elimination in humans appear to be heterochronous in different cortical regions and, in that respect, appears to differ from the rhesus monkey, where they are concurrent. In other respects, including overproduction of synaptic contacts in infancy, persistence of high levels of synaptic density to late childhood or adolescence, the absolute values of maximum and adult synaptic density, and layer specific differences, findings in the human resemble those in rhesus monkeys.
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            Synaptic density in human frontal cortex - developmental changes and effects of aging.

            P Huttenlocher (1979)
            Density of synaptic profiles in layer 3 of middle frontal gyrus was quantitated in 21 normal human brains ranging from newborn to age 90 years. Synaptic profiles could be reliably demonstrated by the phosphotungstic acid method (Bloom and Aghajanian) in tissue fixed up to 36 h postmortem. Synaptic density was constant throughout adult life (ages 16--72 years) with a mean of 11.05 X 10(8) synapses/cu.mm +/- 0.41 S.E.M. There was a slight decline in synaptic density in brains of the aged (ages 74--90 years) with a mean of 9.56 X 10(8) synapses/cu.mm +/- 0.28 S.E.M. in 4 samples (P less than 0.05). Synaptic density in neonatal brains was already high--in the range seen in adults. However, synaptic morphology differed; immature profiles had an irregular presynaptic dense band instead of the separate presynaptic projections seen in mature synapses. Synaptic density increased during infancy, reaching a maximum at age 1--2 years which was about 50% above the adult mean. The decline in synaptic density observed between ages 2--16 years was accompanied by a slight decrease in neuronal density. Human cerebral cortex is one of a number of neuronal systems in which loss of neurons and synapses appears to occur as a late developmental event.
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              Gene expression deficits in a subclass of GABA neurons in the prefrontal cortex of subjects with schizophrenia.

              Takanori Hashimoto, David W Volk, Stephen Eggan … (2003)
              Markers of inhibitory neurotransmission are altered in the prefrontal cortex (PFC) of subjects with schizophrenia, and several lines of evidence suggest that these alterations may be most prominent in the subset of GABA-containing neurons that express the calcium-binding protein, parvalbumin (PV). To test this hypothesis, we evaluated the expression of mRNAs for PV, another calcium-binding protein, calretinin (CR), and glutamic acid decarboxylase (GAD67) in postmortem brain specimens from 15 pairs of subjects with schizophrenia and matched control subjects using single- and dual-label in situ hybridization. Signal intensity for PV mRNA expression in PFC area 9 was significantly decreased in the subjects with schizophrenia, predominantly in layers III and IV. Analysis at the cellular level revealed that this decrease was attributable principally to a reduction in PV mRNA expression per neuron rather than by a decreased density of PV mRNA-positive neurons. In contrast, the same measures of CR mRNA expression were not altered in schizophrenia. These findings were confirmed by findings from cDNA microarray studies using different probes. Across the subjects with schizophrenia, the decrease in neuronal PV mRNA expression was highly associated (r = 0.84) with the decrease in the density of neurons containing detectable levels of GAD67 mRNA. Furthermore, simultaneous detection of PV and GAD67 mRNAs revealed that in subjects with schizophrenia only 55% of PV mRNA-positive neurons had detectable levels of GAD67 mRNA. Given the critical role that PV-containing GABA neurons appear to play in regulating the cognitive functions mediated by the PFC, the selective alterations in gene expression in these neurons may contribute to the cognitive deficits characteristic of schizophrenia.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Schizophr Bull
                Journal ID (publisher-id): Schizophrenia Bulletin
                Journal ID (hwp): schbul
                Title: Schizophrenia Bulletin
                Publisher: Oxford University Press
                ISSN (Print): 0586-7614
                ISSN (Electronic): 1745-1701
                Publication date (Print): January 2008
                Publication date (Electronic): 29 September 2007
                Volume: 34
                Issue: 1
                Pages: 30-36
                Affiliations
                [2 ]Child Psychiatry Branch, National Institute of Mental Health, National Institutes of Health, Building 10, Room 3N202, 10 Center Drive, MSC-1600 Bethesda, MD 20892
                Author notes
                [1 ]To whom correspondence should be addressed; tel: 301-435-4494, fax: 301-402-0296, e-mail: gogtayn@ 123456mail.nih.gov .
                Article
                DOI: 10.1093/schbul/sbm103
                PMC ID: 2632387
                PubMed ID: 17906336
                SO-VID: d4ab4403-33aa-4f27-bd39-a4eebe57db06
                Copyright © Published by Oxford University Press 2007.
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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                Categories
                Subject: Special Theme: Adolescents with Schizophrenia

                ScienceOpen disciplines: Neurology
                Keywords: structural brain imaging,childhood-onset schizophrenia
                Data availability:
                ScienceOpen disciplines: Neurology
                Keywords: structural brain imaging, childhood-onset schizophrenia

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