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    White matter neuron alterations in schizophrenia and related disorders

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    Authors
    Connor, Caroline M.
    Crawford, Benjamin C.
    Akbarian, Schahram
    Student Authors
    Caroline Connor
    UMass Chan Affiliations
    Brudnick Neuropsychiatric Research Institute, Department of Psychiatry
    Document Type
    Journal Article
    Publication Date
    2011-05-10
    Keywords
    Schizophrenia; Neurons; Leukoencephalopathies
    Life Sciences
    Medicine and Health Sciences
    Neuroscience and Neurobiology
    
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    Link to Full Text
    http://dx.doi.org/10.1016/j.ijdevneu.2010.07.236
    Abstract
    Increased density and altered spatial distribution of subcortical white matter neurons (WMNs) represents one of the more well replicated cellular alterations found in schizophrenia and related disease. In many of the affected cases, the underlying genetic risk architecture for these WMN abnormalities remains unknown. Increased density of neurons immunoreactive for Microtubule-Associated Protein 2 (MAP2) and Neuronal Nuclear Antigen (NeuN) have been reported by independent studies, though there are negative reports as well; additionally, group differences in some of the studies appear to be driven by a small subset of cases. Alterations in markers for inhibitory (GABAergic) neurons have also been described. For example, downregulation of neuropeptide Y (NPY) and nitric oxide synthase (NOS1) in inhibitory WMN positioned at the gray/white matter border, as well as altered spatial distribution, have been reported. While increased density of WMN has been suggested to reflect disturbance of neurodevelopmental processes, including neuronal migration, neurogenesis, and cell death, alternative hypotheses-such as an adaptive response to microglial activation in mature CNS, as has been described in multiple sclerosis -should also be considered. We argue that larger scale studies involving hundreds of postmortem specimens will be necessary in order to clearly establish the subset of subjects affected. Additionally, these larger cohorts could make it feasible to connect the cellular pathology to environmental and genetic factors implicated in schizophrenia, bipolar disorder, and autism. These could include the 22q11 deletion (Velocardiofacial/DiGeorge) syndrome, which in some cases is associated with neuronal ectopias in white matter.
    Source
    Int J Dev Neurosci. 2011 May;29(3):325-34. Epub 2010 Aug 4. Link to article on publisher's site
    DOI
    10.1016/j.ijdevneu.2010.07.236
    Permanent Link to this Item
    http://hdl.handle.net/20.500.14038/33151
    PubMed ID
    20691252
    Related Resources
    Link to Article in PubMed
    ae974a485f413a2113503eed53cd6c53
    10.1016/j.ijdevneu.2010.07.236
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