Shared molecular neuropathology across major psychiatric disorders parallels polygenic overlap

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Science  09 Feb 2018:
Vol. 359, Issue 6376, pp. 693-697
DOI: 10.1126/science.aad6469

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  • RE: In silico data-mining in postmortem neuropsychiatric research
    • Sinead M. O'Donovan, Postdoctoral researcher, University of Cincinnati
    • Other Contributors:
      • Adam Funk, Postdoctoral researcher, University of Cincinnati
      • Courtney Sullivan, PhD student, University of Cincinnati
      • Robert McCullumsmith, Associate Professor, University of Cincinnati

    In Shared molecular neuropathology across major psychiatric disorders parallels polygenic overlap (February 9; 359, 6376), the authors conducted meta-analyses of postmortem transcriptome studies, incorporating microarray and RNAseq databases, to effectively exploit an underutilized in silico resource. Gandal et al. applied stringent normalization and network analysis methodologies, addressing many of the intrinsic limitations associated with postmortem tissue and validating the utility of postmortem transcriptome analysis in neuropsychiatric research (1, 2). This approach generated patterns of gene expression that are both common across and unique to prevalent neuropsychiatric disorders.
    Notwithstanding the robust quality control checks applied during analysis, these gene expression data are an amalgam of findings from different cortical regions and multiple cell types (3). Blended, whole tissue samples can mask small changes in expression in a specific cell population or nullify detection of discordant expression of the same gene in different cell types, impeding comprehensive detection of altered gene expression levels. This is a common constraint of region-level gene expression analysis (4).
    Following analysis, modules of genes perturbed in disease were assembled and characterized by cell-type specificity, based on previous RNAseq-derived gene expression enrichment in purified brain cell populations (5). It is notable that the primary focus of this cell-leve...

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    Competing Interests: None declared.
  • RE: proposal of further steps

    Dear Authors,
    Thanks for the research done.
    I have a dipolar disease, my brother had schizophrenia. On my mother side other oncle with same disease. To me it is totally clear that this must have a genetic cause. I have been working for 9 years at EMBL in Heidelberg and have a high interest in the disease. For both my brother and me LiCO3 is a fantastic Medizin. As far as I know it is still not known why. It thus would be interesting if the genetic patterns are "reversed" or not. If Li labelling is possible it would be interesting to see where it attaches. Also a CasCrip therapy is a vision for the future.
    If needed I gladly contribute to your research.
    Best Regards,
    H. v. d. Zandt

    Competing Interests: None declared.

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