Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
8.1
4.9
Journals
IJMS
Special Issues
Advances in Neurogenetics and Neuroimmunology
ijms-logo
Submit to IJMS Review for IJMS Propose a Special Issue

Journal Menu

► Journal Menu

Journal Browser

► Journal Browser
share announcement

Advances in Neurogenetics and Neuroimmunology

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Neurobiology".

Deadline for manuscript submissions: closed (30 September 2023) | Viewed by 7587

Special Issue Editor

Dr. Marwa Zafarullah

E-Mail Website
Guest Editor
College of Biological Sciences, University of California Davis, Davis, CA 95817, USA
Interests: neurodegenerative disorders; genetics; rare complex syndromes; FXTAS; genomics; biomarker discovery; FXS; next-generation sequencing; Intellectual disability
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear colleagues,

Neurogenetics and neuroimmunology are disciplines with their roots in the fields of neuroscience, neurology, genetics, and immunology. The technological advances in these disciplines not only open the window towards a better understanding of the various neurological conditions but also aid our knowledge of how the immune system and genetics influence the nervous system during the development of these disorders. Thus, it is of importance to highlight historical aspects and milestones in these fields and discuss the paradigm shifts that have helped provide novel insights into disease mechanisms. Moreover, the future perspectives including molecular biological studies and experimental models will open new avenues for targeted therapeutic approaches.

It is our pleasure to announce a new Special Issue of the International Journal of Molecular Sciences on “Advances in Neurogenetics and Neuroimmunology.” With this Special Issue, we intend to collect both original contributions and review articles focused on:

i. Research directions towards the identification of complex genetics and the unique immunological pathways involved in the development of various brain disorders;

ii. The investigation of the underlying biochemical and molecular mechanisms with an aim to develop novel targeted therapies;

iii. The ongoing advancements in research and the future perspectives on the transition from the bench to bedside.

Since IJMS is a journal of molecular science, pure clinical studies will not be suitable; however, clinical submissions with biomolecular experiments focusing on the topics mentioned above are welcomed. We encourage you to reach out to us if you have any questions or confusion.

Dr. Marwa Zafarullah
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • neurogenetics
  • neuroimmunology
  • translational research
  • targeted therapeutics
  • brain disorders

Published Papers (3 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

Jump to: Review

13 pages, 782 KiB  
Article
The Impact of BDNF, NTRK2, NGFR, CREB1, GSK3B, AKT, MAPK1, MTOR, PTEN, ARC, and SYN1 Genetic Polymorphisms in Antidepressant Treatment Response Phenotypes
by Marlene Santos, Luis Lima, Serafim Carvalho, Jorge Mota-Pereira, Paulo Pimentel, Dulce Maia, Diana Correia, M. Fátima Barroso, Sofia Gomes, Agostinho Cruz and Rui Medeiros
Int. J. Mol. Sci. 2023, 24(7), 6758; https://doi.org/10.3390/ijms24076758 - 4 Apr 2023
Cited by 7 | Viewed by 2387
Abstract
This study aimed to investigate the influence of genetic variants in neuroplasticity-related genes on antidepressant treatment phenotypes. The BDNF-TrkB signaling pathway, as well as the downstream kinases Akt and ERK and the mTOR pathway, have been implicated in depression and neuroplasticity. However, clinicians [...] Read more.
This study aimed to investigate the influence of genetic variants in neuroplasticity-related genes on antidepressant treatment phenotypes. The BDNF-TrkB signaling pathway, as well as the downstream kinases Akt and ERK and the mTOR pathway, have been implicated in depression and neuroplasticity. However, clinicians still struggle with the unpredictability of antidepressant responses in depressed patients. We genotyped 26 polymorphisms in BDNF, NTRK2, NGFR, CREB1, GSK3B, AKT, MAPK1, MTOR, PTEN, ARC, and SYN1 in 80 patients with major depressive disorder treated according to the Texas Medical Algorithm for 27 months at Hospital Magalhães Lemos, Porto, Portugal. Our results showed that BDNF rs6265, PTEN rs12569998, and SYN1 rs1142636 SNP were associated with treatment-resistant depression (TRD). Additionally, MAPK1 rs6928 and GSK3B rs6438552 gene polymorphisms were associated with relapse. Moreover, we found a link between the rs6928 MAPK1 polymorphism and time to relapse. These findings suggest that the BDNF, PTEN, and SYN1 genes may play a role in the development of TRD, while MAPK1 and GSK3B may be associated with relapse. GO analysis revealed enrichment in synaptic and trans-synaptic transmission pathways and glutamate receptor activity with TRD-associated genes. Genetic variants in these genes could potentially be incorporated into predictive models of antidepressant response. Full article
(This article belongs to the Special Issue Advances in Neurogenetics and Neuroimmunology)
►▼ Show Figures

Figure 1

14 pages, 2508 KiB  
Article
Cadmium Exposure Is Associated with Behavioral Deficits and Neuroimmune Dysfunction in BTBR T+ Itpr3tf/J Mice
by Mohammed M. Alanazi, Mushtaq A. Ansari, Ahmed Nadeem, Sabry M. Attia, Saleh A. Bakheet, Haneen A. Al-Mazroua, Abdullah A. Aldossari, Mohammed M. Almutairi, Thamer H. Albekairi, Marwa H. Hussein, Mohammed A. Al-Hamamah and Sheikh F. Ahmad
Int. J. Mol. Sci. 2023, 24(7), 6575; https://doi.org/10.3390/ijms24076575 - 31 Mar 2023
Cited by 4 | Viewed by 1632
Abstract
Autism spectrum disorders (ASD) are neurobehavioral disabilities characterized by impaired social interactions, poor communication skills, and restrictive/repetitive behaviors. Cadmium is a common heavy metal implicated in ASD. In this study, we investigated the effects of Cd exposure on BTBR T+ Itpr3tf/J (BTBR) mice, [...] Read more.
Autism spectrum disorders (ASD) are neurobehavioral disabilities characterized by impaired social interactions, poor communication skills, and restrictive/repetitive behaviors. Cadmium is a common heavy metal implicated in ASD. In this study, we investigated the effects of Cd exposure on BTBR T+ Itpr3tf/J (BTBR) mice, an ASD model. We looked for changes in repetitive behaviors and sociability through experiments. We also explored the molecular mechanisms underlying the effects of Cd exposure, focusing on proinflammatory cytokines and pathways. Flow cytometry measured IL-17A-, IL-17F-, IL-21-, TNF-α-, STAT3-, and RORγt-expressing CD4+ T cells from the spleens of experimental mice. We then used RT-PCR to analyze IL-17A, IL-17F, IL-21, TNF-α, STAT3, and RORγ mRNA expression in the brain. The results of behavioral experiments showed that Cd exposure significantly increased self-grooming and marble-burying in BTBR mice while decreasing social interactions. Cd exposure also significantly increased the number of CD4+IL-17A+, CD4+IL-17F+, CD4+IL-21+, CD4+TNF-α+, CD4+STAT3+, and CD4+RORγt+ cells, while upregulating the mRNA expression of the six molecules in the brain. Overall, our results suggest that oral exposure to Cd aggravates behavioral and immune abnormalities in an ASD animal model. These findings have important implications for ASD etiology and provide further evidence of heavy metals contributing to neurodevelopmental disorders through proinflammatory effects. Full article
(This article belongs to the Special Issue Advances in Neurogenetics and Neuroimmunology)
►▼ Show Figures

Figure 1

Review

Jump to: Research

26 pages, 2204 KiB  
Review
Seeing Neurodegeneration in a New Light Using Genetically Encoded Fluorescent Biosensors and iPSCs
by David Stellon, Jana Talbot, Alex W. Hewitt, Anna E. King and Anthony L. Cook
Int. J. Mol. Sci. 2023, 24(2), 1766; https://doi.org/10.3390/ijms24021766 - 16 Jan 2023
Viewed by 2942
Abstract
Neurodegenerative diseases present a progressive loss of neuronal structure and function, leading to cell death and irrecoverable brain atrophy. Most have disease-modifying therapies, in part because the mechanisms of neurodegeneration are yet to be defined, preventing the development of targeted therapies. To overcome [...] Read more.
Neurodegenerative diseases present a progressive loss of neuronal structure and function, leading to cell death and irrecoverable brain atrophy. Most have disease-modifying therapies, in part because the mechanisms of neurodegeneration are yet to be defined, preventing the development of targeted therapies. To overcome this, there is a need for tools that enable a quantitative assessment of how cellular mechanisms and diverse environmental conditions contribute to disease. One such tool is genetically encodable fluorescent biosensors (GEFBs), engineered constructs encoding proteins with novel functions capable of sensing spatiotemporal changes in specific pathways, enzyme functions, or metabolite levels. GEFB technology therefore presents a plethora of unique sensing capabilities that, when coupled with induced pluripotent stem cells (iPSCs), present a powerful tool for exploring disease mechanisms and identifying novel therapeutics. In this review, we discuss different GEFBs relevant to neurodegenerative disease and how they can be used with iPSCs to illuminate unresolved questions about causes and risks for neurodegenerative disease. Full article
(This article belongs to the Special Issue Advances in Neurogenetics and Neuroimmunology)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-3
Back to TopTop