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5.1
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Journals
Genes
Special Issues
Genetic and Epigenetic Factors of Mental Disorders
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Genetic and Epigenetic Factors of Mental Disorders

A special issue of Genes (ISSN 2073-4425). This special issue belongs to the section "Human Genomics and Genetic Diseases".

Deadline for manuscript submissions: closed (15 June 2016) | Viewed by 6778

Special Issue Editor

Dr. Huiping Zhang

E-Mail Website
Guest Editor
Division of Human Genetics, Department of Psychiatry, Yale University School of Medicine, 950 Campbell Avenue, West Haven, CT 06516, USA
Interests: psychiatric genetics; substance dependence; genetic and epigenetic studies; DNA methylation; microRNA regulation; functional genomics; stem cell; mouse models

Special Issue Information

Dear Colleagues,

Mental disorders are common health problems that impact an individual’s thinking, feeling or mood and thus influence his/her social and daily life. Genetic variations and environmental factors may have a combined effect on risk of mental disorders. Inherited epigenetic marks or altered epigenetic status resulting from environmental exposures or certain lifestyles may also affect an individual’s vulnerability to mental disorders. The state-of-the-art microarray and next-generation sequencing technologies allow us to identify mental disorders-associated genetic and epigenetic marks at the genome-wide level. Advances in animal or cell models facilitate functional studies of mental disorders-associated genes/variants. Identification of genetic and epigenetic risk factors for mental disorders will help developing personalized medications.

This special issue provides a forum for experimental and clinical studies to explore the role of genetics and epigenetics in mental disorders, such as anxiety disorder, attention deficit hyperactivity disorder, autism, bipolar disorder, depressive disorder, eating disorder, obsessive-compulsive disorder, schizophrenia, and substance abuse/dependence.

This special issue of Genes welcomes reviews and original articles covering recent research on mental disorders with the use of study approaches such as candidate gene or genome-wide genetic and epigenetic studies, next-generation sequencing, functional genomics studies, pharmacogenetic studies, and gene-environment interaction analysis.

Dr. Huiping Zhang
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Genes is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • Mental disorders
  • Complex genetic disorders
  • Genetics
  • Epigenetics
  • Association analysis
  • Functional polymorphisms
  • Gene regulation
  • Next-generation sequecing
  • DNA methylation
  • Histone modifications
  • Chromosome remodeling
  • Non-coding RNA regulation

Published Papers (1 paper)

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Research

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Article
Imbalance between Glutamate and GABA in Fmr1 Knockout Astrocytes Influences Neuronal Development
by Lu Wang, Yan Wang, Shimeng Zhou, Liukun Yang, Qixin Shi, Yujiao Li, Kun Zhang, Le Yang, Minggao Zhao and Qi Yang
Genes 2016, 7(8), 45; https://doi.org/10.3390/genes7080045 - 10 Aug 2016
Cited by 19 | Viewed by 6405
Abstract
Fragile X syndrome (FXS) is a form of inherited mental retardation that results from the absence of the fragile X mental retardation protein (FMRP), the product of the Fmr1 gene. Numerous studies have shown that FMRP expression in astrocytes is important in the [...] Read more.
Fragile X syndrome (FXS) is a form of inherited mental retardation that results from the absence of the fragile X mental retardation protein (FMRP), the product of the Fmr1 gene. Numerous studies have shown that FMRP expression in astrocytes is important in the development of FXS. Although astrocytes affect neuronal dendrite development in Fmr1 knockout (KO) mice, the factors released by astrocytes are still unclear. We cultured wild type (WT) cortical neurons in astrocyte-conditioned medium (ACM) from WT or Fmr1 KO mice. Immunocytochemistry and Western blotting were performed to detect the dendritic growth of both WT and KO neurons. We determined glutamate and γ-aminobutyric acid (GABA) levels using high-performance liquid chromatography (HPLC). The total neuronal dendritic length was reduced when cultured in the Fmr1 KO ACM. This neurotoxicity was triggered by an imbalanced release of glutamate and GABA from Fmr1 KO astrocytes. We found increased glutaminase and GABA transaminase (GABA-T) expression and decreased monoamine oxidase B expression in Fmr1 KO astrocytes. The elevated levels of glutamate contributed to oxidative stress in the cultured neurons. Vigabatrin (VGB), a GABA-T inhibitor, reversed the changes caused by glutamate and GABA release in Fmr1 KO astrocytes and the abnormal behaviors in Fmr1 KO mice. Our results indicate that the imbalance in the astrocytic glutamate and GABA release may be involved in the neuropathology and the underlying symptoms of FXS, and provides a therapeutic target for treatment. Full article
(This article belongs to the Special Issue Genetic and Epigenetic Factors of Mental Disorders)
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