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2 results

  • Gene expression in peripheral blood in treatment-free major depression

  • Alfredo B. Cuellar-Barboza, Jorge A. Sánchez-Ruiz, Iram P. Rodriguez-Sanchez, Sarai González, Geovana Calvo, José Lugo, Antonio Costilla-Esquivel, Laura E. Martínez, Marisol Ibarra-Ramirez
  • Journal:
    Acta Neuropsychiatrica / Volume 32 / Issue 3 / June 2020
    Published online by Cambridge University Press:
    10 February 2020, pp. 135-144
  • Background:

    Peripheral gene expression of several molecular pathways has been studied in major depressive disorder (MDD) with promising results. We sought to investigate some of these genes in a treatment-free Latino sample of Mexican descent.

    Material and Methods:

    The sample consisted of 50 MDD treatment-free cases and 50 sex and age-matched controls. Gene expression of candidate genes of neuroplasticity (BDNF, p11, and VGF), inflammation (IL1A, IL1B, IL4, IL6, IL7, IL8, IL10, MIF, and TNFA), the canonical Wnt signaling pathway (TCF7L2, APC, and GSK3B), and mTOR, was compared in cases and controls. RNA was obtained from blood samples. We used bivariate analyses to compare subjects versus control mean mRNA quantification of target genes and lineal regression modelling to test for effects of age and body mass index on gene expression.

    Results:

    Most subjects were female (66%) with a mean age of 26.7 (SD 7.9) years. Only GSK3B was differentially expressed between cases and controls at a statistically significant level (p = 0.048). TCF7L-2 showed the highest number of correlations with MDD-related traits, yet these were modest in size.

    Discussion:

    GSK3B encodes a moderator of the canonical Wnt signaling pathway. It has a role in neuroplasticity, neuroprotection, depression, and other psychiatric phenotypes. We found that adding population diversity has the potential to elicit distinct peripheral gene expression markers in MDD and MDD-related traits. However, our results should only be considered as hypothesis-generating research that merits further replication in larger cohorts of similar ancestry.

  • Chapter 3 - Human embryology

  • from Section 1 - General principles
  • Edited by Mark D. Kilby, Anthony Johnson, Baylor College of Medicine, Texas, Dick Oepkes
  • Book:
    Fetal Therapy
    Published online:
    05 February 2013
    Print publication:
    13 December 2012, pp 24-38

  • Summary

    There are five major signaling pathways that control embryogenesis, comprising the Hedgehog, Wnt, TGFβ/Bmp, Notch, and fibroblast growth factor (FGF) signaling families. Together these control cell proliferation, cell survival, changes in cell shape, migration, adhesion, and cell differentiation. Mutation in components of these pathways results in a number of human syndromes. This chapter discusses the five key signaling pathways that control embryonic development. It describes the various roles, mechanisms of action of each pathway and highlights syndromes that are due to mutations in components of these signaling pathways. The chapter explains how mutations in transcription factors, matrix molecules, and epigenetic factors can affect embryonic development. During embryonic development, the vertebrae and axial musculature develop from somites, which are epithelial balls that periodically bud off from the unsegmented paraxial mesoderm. Deregulation of the notch pathway affects somite development by deregulating the clock and preventing the formation of boundaries.