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Annotation

Dracheva S, Davis KL, Chin B, Woo DA, Schmeidler J, Haroutunian V. Myelin-associated mRNA and protein expression deficits in the anterior cingulate cortex and hippocampus in elderly schizophrenia patients. Neurobiol Dis . 2005 Oct 4 ; PubMed Abstract

Comments on Related News
Related News: CNP Findings Strengthen Oligodendrocyte Link to Schizophrenia

Comment by:  Hans W. Moises
Submitted 24 January 2006 Posted 24 January 2006
  I recommend the Primary Papers

This is another important study supporting the glial growth factors deficiency and synaptic destabilization hypothesis of schizophrenia we proposed in 2002 (Moises et al., 2002). The glial synaptic destabilization hypothesis is based on the landmark 1997 paper by Pfrieger and Barres and the tripartite synapse model suggested by Philip Haydon and coworkers (Araque et al., 1999; Pascual et al., 2005). In reference to its underlying principle, the glial growth factors deficiency and synaptic destabilization hypothesis might also more conveniently and briefly be designated as the weakened tripartite-synapse hypothesis of schizophrenia.

References:
Moises HW, Zoega T, Gottesman II. The glial growth factors deficiency and synaptic destabilization hypothesis of schizophrenia. BMC Psychiatry. 2002;2:8. Abstract

Moises HW, Gottesman II. Does glial asthenia predispose to schizophrenia? Arch Gen Psychiatry 2004; 61:1170. Abstract

Pfrieger FW, Barres BA. Synaptic efficacy enhanced by glial cells in vitro. Science. 1997;277:1684-7. Abstract

Araque A, Parpura V, Sanzgiri RP, Haydon PG. Tripartite synapses: glia, the unacknowledged partner. Trends Neurosci. 1999; 22:208-15. Abstract

Pascual O, Casper KB, Kubera C, Zhang J, Revilla-Sanchez R, Sul JY, Takano H, Moss SJ, McCarthy K, Haydon PG. Astrocytic purinergic signaling coordinates synaptic networks. Science 2005; 310: 113-6. Abstract

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Related News: CNP Findings Strengthen Oligodendrocyte Link to Schizophrenia

Comment by:  Daniel StewartKenneth Davis
Submitted 31 January 2006 Posted 31 January 2006

Peirce's paper is an exciting addition to the white matter hypothesis in schizophrenia. (Note: many of the authors of this paper are colleagues of ours at the Conte Center investigating white matter in schizophrenia at Mount Sinai.) As noted in the news story, findings from a number of different areas are beginning to come together in support of the white matter hypothesis in schizophrenia. Genetic findings in myelin-related genes, as outlined and referenced above, are demonstrating increased susceptibility to schizophrenia. Imaging findings from diffusion tensor studies are demonstrating abnormalities across multiple brain areas (reviewed in Kubicki et al., 2005), with more recent studies showing that specific white matter tracts are not only abnormal in schizophrenia, but are associated with symptomatology and cognitive deficits (Kubicki et al., 2002;   Read more


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Related News: CNP Findings Strengthen Oligodendrocyte Link to Schizophrenia

Comment by:  William Honer
Submitted 4 March 2006 Posted 5 March 2006
  I recommend the Primary Papers

The Peirce et al. paper represents an important contribution to understanding the possible mechanisms through which genetic risk factors could contribute to the pathophysiology of schizophrenia. Studies of SNPs in candidate genes for schizophrenia are most clearly related to mechanism when the SNP changes amino acid sequence (rarely), or when the SNP changes mRNA expression (commonly postulated, but less often demonstrated). Studies combining SNP and mRNA analyses are challenging, and Peirce et al. provide a novel approach—by measuring the relative amount of mRNA expressed from the variant and the wild-type alleles in brain tissue from heterozygotes. They demonstrated relatively reduced expression from the variant allele. It must be noted however, that these studies were carried out in brain tissue from individuals described as being “free from psychiatric or neurological disorder at time of death” (not schizophrenia samples as suggested by the SRF news story [Editor's note: since corrected]), and the total expression of CNP mRNA was not determined. While CNP mRNA...  Read more


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