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Genes
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Genetics of Neuropsychiatric Disorders
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Genetics of Neuropsychiatric Disorders

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

Deadline for manuscript submissions: 25 October 2025 | Viewed by 1294

Special Issue Editors

Dr. Melloni Cook

E-Mail Website
Guest Editor
Department of Psychology, University of Memphis, Memphis, TN 38152, USA
Interests: genetics of complex traits; behavioral genetics; anxiety; stress; learning and memory; stress/ethanol interactions
Dr. Kristin Hamre

E-Mail Website
Guest Editor
Department of Anatomy and Neurobiology, University of Tennessee Health Science Center, Memphis, TN 38163, USA
Interests: genetics of substance abuse particularly following developmental exposure; genetics of behavioral traits; interaction of sex and genetics

Special Issue Information

Dear Colleagues,

Neuropsychiatric disorders are pervasive and can be debilitating. Further, individuals with these disorders often have delayed diagnoses or present comorbid disorders. Treatment options remain limited, are often associated with undesirable side effects, and have significant nonresponse rates. As many of these disorders involve a genetic component, identifying and characterizing genetic influences on these disorders may help in discovering biomarkers for early/better detection, characterizing causal variants, pinpointing novel pathways as targets for the development of therapeutics, and determining whether comorbid disorders have common underlying mechanisms. Thanks to conceptual, technical, and bioinformatic advances, we are better positioned to understand these complex disorders.

In the Special Issue of Genes, we will highlight recent discoveries in the genetics of neuropsychiatric disorders, including major depressive disorder, schizophrenia, post-traumatic stress disorder, anxiety disorders, addiction, stress-related disorders, and their related phenotypes. We welcome review and original articles in the following areas: behavioral neuroscience, gene expression analyses, epigenetics, optogenetics, and miRNA expression, among others. Works employing animal models, clinical populations, or human tissues are welcome.

Dr. Melloni Cook
Dr. Kristin Hamre
Guest Editors

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

  • major depressive disorder
  • schizophrenia
  • post-traumatic stress disorder
  • addiction
  • alcohol
  • drugs
  • anxiety disorder
  • stress-related disorders
  • genes
  • epigenetics
  • mRNA
  • optogenetics
  • miRNA
  • causal variant

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Published Papers (1 paper)

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Research

16 pages, 2809 KiB  
Article
Neuromolecular Basis of Impaired Conditioned Taste Aversion Acquisition in Valproate-Induced Rat Model of Autism Spectrum Disorder
by Tapasya Pal, Savannah Harvey, Allen S. Levine, Pawel K. Olszewski and Anica Klockars
Genes 2025, 16(2), 203; https://doi.org/10.3390/genes16020203 - 7 Feb 2025
Viewed by 994
Abstract
Background/Objectives: Autism spectrum disorder (ASD), defined by social, behavioral, and cognitive anomalies, is also associated with dysregulated appetite. ASD individuals, often described as “picky eaters”, exhibit restricted dietary preferences and a pronounced avoidance of novel foods. This suggests that the perceived safety of [...] Read more.
Background/Objectives: Autism spectrum disorder (ASD), defined by social, behavioral, and cognitive anomalies, is also associated with dysregulated appetite. ASD individuals, often described as “picky eaters”, exhibit restricted dietary preferences and a pronounced avoidance of novel foods. This suggests that the perceived safety of specific tastants may be a crucial determinant of dietary acceptance in ASD. Here, we explore the hypothesis that conditioned taste aversion (CTA), a learned avoidance of foods whose intake promotes sickness, is exacerbated in ASD. Methods: We assessed the magnitude of a lithium chloride (LiCl)-induced CTA in the valproic acid (VPA) rat model of autism versus in healthy control rats. We also examined the effect of a standard 3 mEq LiCl dose on transcript and neuronal activation changes in brain circuits mediating feeding behavior and associative learning. Results: Surprisingly, we found that while 3 mEq LiCl induced CTA in healthy controls, even the 6 mEq dose was ineffective in generating aversion in VPA rats. LiCl at 3 mEq affected c-Fos immunoreactivity in the hypothalamus and amygdala in controls, whereas in VPA rats it did not produce any c-Fos changes. Gene expression analysis of feeding-related genes (AgRP, NPY, OXT) and those involved in regulating stress and anxiety (DOR and MC3R) were differentially regulated in the VPA rats. Interestingly, transcripts for COMT1, AgRP, OXT, and MC3R were downregulated in saline-treated VPA rats compared to saline-treated controls. Conclusions: We conclude that VPA rats show blunted CTA responsiveness, which is reflected by a differential impact of LiCl on circuits that promote the acquisition of CTA in healthy versus autistic individuals. Full article
(This article belongs to the Special Issue Genetics of Neuropsychiatric Disorders)
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