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      False data, positive results in neurobiology: moving beyond the epigenetics of blood and saliva samples in mental disorders

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          Abstract

          Many psychiatric diseases are influenced by a set of several genetic and environmental factors that genetics alone cannot explain. Specifically, in schizophrenia and bipolar disorder the absence of consistently replicated genetic effects together with evidence for lasting changes in gene expression after environmental exposures suggest a role of epigenetic mechanisms in its pathophysiological mechanisms. In this field, the presence of positive results could potentially uncover molecular mechanisms of deregulated gene expression in these complex disorders. In this commentary we have reviewed the positive data obtained over the last 5 years from the scientific literature published in PubMed and we have shown that these results are based on peripheral samples (blood, saliva and other fluids) that do not allow us to obtain reliable and/or valid results, under any circumstances. Finally, we highlight the need to employ human brain samples in the epigenetic study of mental disorders.

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          Most cited references13

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          Principles and challenges of genomewide DNA methylation analysis.

          Methylation of cytosine bases in DNA provides a layer of epigenetic control in many eukaryotes that has important implications for normal biology and disease. Therefore, profiling DNA methylation across the genome is vital to understanding the influence of epigenetics. There has been a revolution in DNA methylation analysis technology over the past decade: analyses that previously were restricted to specific loci can now be performed on a genome-scale and entire methylomes can be characterized at single-base-pair resolution. However, there is such a diversity of DNA methylation profiling techniques that it can be challenging to select one. This Review discusses the different approaches and their relative merits and introduces considerations for data analysis.
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            Dynamic reprogramming of DNA methylation in the early mouse embryo.

            Dynamic epigenetic modification of the genome occurs during early development of the mouse. Active demethylation of the paternal genome occurs in the zygote, followed by passive demethylation during cleavage stages, and de novo methylation, which is thought to happen after implantation. We have investigated these processes by using indirect immunofluorescence with an antibody to 5-methyl cytosine. In contrast to previous work, we show that demethylation of the male pronucleus is completed within 4 h of fertilisation. This activity is intricately linked with and not separable from pronucleus formation. In conditions permissive for polyspermy, up to five male pronuclei underwent demethylation in the same oocyte. Paternal demethylation in fertilised oocytes deficient for MBD2, the only candidate demethylase, occurred normally. Passive loss of methylation occurred in a stepwise fashion up to the morulae stage without any evidence of spatial compartmentalisation. De novo methylation was observed specifically in the inner cell mass (ICM) but not in the trophectoderm of the blastocyst and hence may have an important role in early lineage specification. This is the first complete and detailed analysis of the epigenetic reprogramming cycle during preimplantation development. The three phases of methylation reprogramming may have roles in imprinting, the control of gene expression, and the establishment of nuclear totipotency.
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              Do Pressures to Publish Increase Scientists' Bias? An Empirical Support from US States Data

              The growing competition and “publish or perish” culture in academia might conflict with the objectivity and integrity of research, because it forces scientists to produce “publishable” results at all costs. Papers are less likely to be published and to be cited if they report “negative” results (results that fail to support the tested hypothesis). Therefore, if publication pressures increase scientific bias, the frequency of “positive” results in the literature should be higher in the more competitive and “productive” academic environments. This study verified this hypothesis by measuring the frequency of positive results in a large random sample of papers with a corresponding author based in the US. Across all disciplines, papers were more likely to support a tested hypothesis if their corresponding authors were working in states that, according to NSF data, produced more academic papers per capita. The size of this effect increased when controlling for state's per capita R&D expenditure and for study characteristics that previous research showed to correlate with the frequency of positive results, including discipline and methodology. Although the confounding effect of institutions' prestige could not be excluded (researchers in the more productive universities could be the most clever and successful in their experiments), these results support the hypothesis that competitive academic environments increase not only scientists' productivity but also their bias. The same phenomenon might be observed in other countries where academic competition and pressures to publish are high.
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                Author and article information

                Contributors
                ariel.cariaga@uah.es
                raul.alelu@uah.es
                Journal
                J Negat Results Biomed
                J Negat Results Biomed
                Journal of Negative Results in Biomedicine
                BioMed Central (London )
                1477-5751
                12 December 2016
                12 December 2016
                2016
                : 15
                : 21
                Affiliations
                [1 ]Laboratory for Neuroscience of Mental Disorders Elena Pessino, Department of Medicine and Medical Specialties, School of Medicine, Alcalá University, Madrid, Spain
                [2 ]Department of Psychiatry, Ramón y Cajal Hospital, IRYCIS, Madrid, Spain
                Article
                64
                10.1186/s12952-016-0064-x
                5151128
                27938391
                3df3d9b6-0acc-474b-9564-73cbdc7f2ad6
                © The Author(s). 2016

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                : 14 July 2016
                : 8 November 2016
                Funding
                Funded by: Canis Majoris Foundation
                Categories
                Commentary
                Custom metadata
                © The Author(s) 2016

                Life sciences
                epigenetics,positive results,peripheral samples,human brain,neurobiology,schizophrenia,bipolar disorder

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