Elsevier

Schizophrenia Research

Volume 193, March 2018, Pages 453-455
Schizophrenia Research

Letter to the Editor
Early trauma and clinical features of schizophrenia cases influenced by the BDNF Val66Met allele

https://doi.org/10.1016/j.schres.2017.06.061Get rights and content

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Role of the funding source

CNPq is a public Brazilian agency and its support is a fellowship for the first author's Post doctorate.

Contributors

André B. Veras, MD, PhD: First author. Full writing of the manuscript, tables preparation, statistical analysis and text review.

Clayton Peixoto, MSPH: Text writing and review.

Julie Walsh Messinger, PhD: Statistical analysis and tables preparation.

Mara Getz, BS: Text writing and text review.

Raymond Goetz, PhD: Statistical analysis and tables preparation.

Peter Buckley, MD: Mentoring and text review.

Moses Chao, PhD: Genetic analysis, mentoring and text review.

Antonio E. Nardi, MD, PhD: Mentoring

Conflict of interest

The authors declare no conflicts of interest related to the present manuscript.

Acknowledgements

The present work was made with the support of CNPq, Conselho Nacional de Desenvolvimento Cientifico e Tecnologico, Brazil (150289/2017-0).

References (10)

There are more references available in the full text version of this article.

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  • Intermediation of perceived stress between early trauma and plasma M/P ratio levels in obsessive-compulsive disorder patients

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    The abnormalities in the conversion of proBDNF to mBDNF is essential to several physiological cycles(Yoshida et al., 2012). Massive evidence suggested that adult BDNF level was affected by early trauma(de Baumont et al., 2019; Marusak et al., 2016; Veras et al., 2018). Whether to the adults or not, a history of early trauma was evidently related to reduced BDNF levels in patients with multiple psychiatric disorders(Benedetti et al., 2017; Dimitriadis et al., 2019; Kavurma et al., 2017).

  • Traumatic experiences and cognitive profiles of schizophrenia cases influenced by the BDNF Val66met polymorphism

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    We previously demonstrated that emotional trauma was significantly related to the severity of general psychopathology symptoms in schizophrenia cases harboring the methionine (Met) allele of brain-derived neurotrophic factor (BDNF) Val66Met polymorphism (Veras et al., 2018).

  • Transcriptomic analysis reveals oxidative phosphorylation activation in an adolescent social isolation rat model

    2018, Brain Research Bulletin
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    SCZ is a psychiatric disorder associated with various genetic and environmental factors. Clinical studies indicate that neurotransmitters (Barr et al., 2004; Yang and Tsai, 2017), neurotrophic factors (Pillai et al., 2017; Veras et al., 2017) and inflammatory factors (Muller, 2017; Pandey et al., 2017) contribute to the comprehensive pathogenesis of SCZ. Recently, an increasing number of animal models have been established to explore the mechanisms of SCZ (Jones et al., 2011), such as maternal separation (Lapiz et al., 2003), maternal immune activation, isolation rearing (Muchimapura et al., 2002, 2003; Fone and Porkess, 2008; Marsden et al., 2011), and drug-induced (Shao et al., 2010; Seillier et al., 2013; Horska et al., 2017) models.

  • Telomere length and early trauma in schizophrenia

    2018, Schizophrenia Research
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    Early trauma exposure is a major risk factor for schizophrenia (Heins et al., 2011; Ruby et al., 2014; Varese et al., 2012), which is furthermore associated with clinical features in the disease, particularly with treatment refractory psychotic symptoms, including auditory hallucinations and command hallucinations (Carr et al., 2013; Heins et al., 2011; Rajkumar, 2015; Read et al., 2005; Ruby et al., 2017; Van Os et al., 2008; Varese et al., 2012). There are a number of possible pathways that could explain the relationship of early trauma to the development of schizophrenia (Read et al., 2001; Ruby et al., 2014; Veras et al., 2018) but none are yet shown to explain the association. One possible mechanism is the shortening telomere lengths by trauma.

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