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Molecular Advances in Mental Health and Disorders

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 20 September 2025 | Viewed by 2398

Special Issue Editor


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Guest Editor
1. Department of Psychiatry, University Hospital, Faculty of Medicine, University of Bonn, Bonn, Germany
2. Institute of Human Genetics, University Hospital, Faculty of Medicine, University of Bonn, Bonn, Germany
Interests: genetics of mental health disorders; functional screens; multiomics; lipidomics

Special Issue Information

Dear Colleagues,

Today, the molecular basis of mental health disorders is still incompletely understood. Yet, it is this lack of an in-depth understanding of the pathophysiology underlying these disorders that presents one of the most important hurdles to new therapeutic and more precise treatment strategies. At the same time, recent years have seen great technological advances in many different pieces of the molecular puzzles in the way that molecular questions can be addressed.

This special issue entitled “Molecular Advances in Mental Health Disorders” seeks to shed light on novel molecular aspects of mental health disorders ranging from autism spectrum disorder to post traumatic stress disorder and from depression phenotypes to addictive disorders. It also includes mental health phenotypes in somatic disorders. Molecular advances can pertain to basic science research just as much as to clinical aspects. This special issue invites works on technological and methodological advances in the analysis of molecular processes in the context of mental health disorders. Further, “molecular advances” can describe the decryption of molecular processes underlying the pathophysiology of mental health disorders using model systems, but also the advances based on strategies rooted in molecular epidemiology and -omics in clinical and population-based cohorts.

Dr. Eva Christina Schulte
Guest Editor

Manuscript Submission Information

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Keywords

  • molecular studies
  • mental health disorders
  • model systems
  • molecular epidemiology
  • omics
 
 

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Published Papers (1 paper)

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Research

19 pages, 4708 KiB  
Article
ANKK1 Is a Wnt/PCP Scaffold Protein for Neural F-ACTIN Assembly
by Laura Domínguez-Berzosa, Lara Cantarero, María Rodríguez-Sanz, Gemma Tort, Elena Garrido, Johanna Troya-Balseca, María Sáez, Xóchitl Helga Castro-Martínez, Sara Fernandez-Lizarbe, Edurne Urquizu, Enrique Calvo, Juan Antonio López, Tomás Palomo, Francesc Palau and Janet Hoenicka
Int. J. Mol. Sci. 2024, 25(19), 10705; https://doi.org/10.3390/ijms251910705 - 4 Oct 2024
Viewed by 1822
Abstract
The TaqIA polymorphism is a marker of both the Ankyrin Repeat and Kinase Domain containing I gene (ANKK1) encoding a RIP-kinase, and the DRD2 gene for the dopamine receptor D2. Despite a large number of studies of TaqIA in [...] Read more.
The TaqIA polymorphism is a marker of both the Ankyrin Repeat and Kinase Domain containing I gene (ANKK1) encoding a RIP-kinase, and the DRD2 gene for the dopamine receptor D2. Despite a large number of studies of TaqIA in addictions and other psychiatric disorders, there is difficulty in interpreting this genetic phenomenon due to the lack of knowledge about ANKK1 function. In SH-SY5Y neuroblastoma models, we show that ANKK1 interacts with the synapse protein FERM ARH/RhoGEF and Pleckstrin Domain 1 (FARP1), which is a guanine nucleotide exchange factor (GEF) of the RhoGTPases RAC1 and RhoA. ANKK1–FARP1 colocalized in F-ACTIN-rich structures for neuronal maturation and migration, and both proteins activate the Wnt/PCP pathway. ANKK1, but not FARP1, promotes neuritogenesis, and both proteins are involved in neuritic spine outgrowth. Notably, the knockdown of ANKK1 or FARP1 affects RhoGTPases expression and neural differentiation. Additionally, ANKK1 binds WGEF, another GEF of Wnt/PCP, regulating its interaction with RhoA. During neuronal differentiation, ANKK1–WGEF interaction is downregulated, while ANKK1–FARP1 interaction is increased, suggesting that ANKK1 recruits Wnt/PCP components for bidirectional control of F-ACTIN assembly. Our results suggest a brain structural basis in TaqIA-associated phenotypes. Full article
(This article belongs to the Special Issue Molecular Advances in Mental Health and Disorders)
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