Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
7.8
5.6
Journals
IJMS
Special Issues
Molecular Mechanism in Movement Disorders and Neurotransmitter Diseases
ijms-logo
Submit to IJMS Review for IJMS Propose a Special Issue

Journal Menu

► Journal Menu

Journal Browser

► Journal Browser
share announcement

Molecular Mechanism in Movement Disorders and Neurotransmitter Diseases

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 (31 January 2022) | Viewed by 8763

Special Issue Editor

Prof. Dr. Wang-Tso Lee

E-Mail Website
Guest Editor
1. Department of Pediatric Neurology, National Taiwan University Children’s Hospital, Taipei 100, Taiwan
2. Graduate Institute of Brain and Mind Sciences, National Taiwan University College of Medicine, Taipei 100, Taiwan
Interests: epilepsy; movement disorders; neurotransmitter diseases; neurometabolic diseases; neurodevelopmental diseases
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Movement disorders are an important group of neurological diseases in children. They include developmental movement disorders, hyperkinetic movement disorders, hypokinetic movement disorders, and paroxysmal movement disorders. Many movement disorders may also be associated with other neurological diseases, such as epilepsy or neurometabolic diseases. Neurotransmitter diseases are another group of neurological diseases that may be associated with different movement disorders in children. The treatment response to medications may be different in different movement disorders and neurotransmitter diseases. Therefore, it is necessary to investigate the potential mechanisms leading to the primary and secondary movement disorders.

The potential mechanisms of movement disorders or neurotransmitter diseases may be related to changes in neurotransmitters or in the synthesis of neurotransmitters. However, some genetic mutations in epilepsy or neurodevelopmental disorders may also affect some signal transduction pathways, leading to the development of movement disorders. A better understanding of the potential mechanisms and the changes to the signal transduction pathways may be of some help to the treatment of these diseases.

This Special Issue, “Molecular Mechanisms of Movement Disorders and Neurotransmitter Diseases”, will focus on potential molecular mechanisms. We hope that this Special Issue will provide a platform for enhancing research on movement disorders.

Prof. Dr. Wang-Tso Lee
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

  • movement disorders
  • neurotransmitter diseases
  • neurometabolic diseases
  • neurodevelopmental diseases
  • dystonia
  • parkinsonism
  • chorea
  • dyskinesia
  • myoclonus
  • paroxysmal dyskinesia
  • hereditary spastic paraplegia
  • ataxia
  • tremor

Published Papers (2 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:

Review

13 pages, 1486 KiB  
Review
Revisiting the Role of Astrocytic MAOB in Parkinson’s Disease
by Min-Ho Nam, Moonsun Sa, Yeon Ha Ju, Mingu Gordon Park and C. Justin Lee
Int. J. Mol. Sci. 2022, 23(8), 4453; https://doi.org/10.3390/ijms23084453 - 18 Apr 2022
Cited by 12 | Viewed by 4925
Abstract
Monoamine oxidase-B (MAOB) has been believed to mediate the degradation of monoamine neurotransmitters such as dopamine. However, this traditional belief has been challenged by demonstrating that it is not MAOB but MAOA which mediates dopamine degradation. Instead, MAOB mediates the aberrant synthesis of [...] Read more.
Monoamine oxidase-B (MAOB) has been believed to mediate the degradation of monoamine neurotransmitters such as dopamine. However, this traditional belief has been challenged by demonstrating that it is not MAOB but MAOA which mediates dopamine degradation. Instead, MAOB mediates the aberrant synthesis of GABA and hydrogen peroxide (H2O2) in reactive astrocytes of Parkinson’s disease (PD). Astrocytic GABA tonically suppresses the dopaminergic neuronal activity, whereas H2O2 aggravates astrocytic reactivity and dopaminergic neuronal death. Recently discovered reversible MAOB inhibitors reduce reactive astrogliosis and restore dopaminergic neuronal activity to alleviate PD symptoms in rodents. In this perspective, we redefine the role of MAOB for the aberrant suppression and deterioration of dopaminergic neurons through excessive GABA and H2O2 synthesis of reactive astrocytes in PD. Full article
(This article belongs to the Special Issue Molecular Mechanism in Movement Disorders and Neurotransmitter Diseases)
►▼ Show Figures

Figure 1

15 pages, 2497 KiB  
Review
Understanding the Molecular Mechanisms of Succinic Semialdehyde Dehydrogenase Deficiency (SSADHD): Towards the Development of SSADH-Targeted Medicine
by Henry H. C. Lee, Gabrielle E. McGinty, Phillip L. Pearl and Alexander Rotenberg
Int. J. Mol. Sci. 2022, 23(5), 2606; https://doi.org/10.3390/ijms23052606 - 26 Feb 2022
Cited by 13 | Viewed by 3374
Abstract
Succinic semialdehyde dehydrogenase deficiency (SSADHD) is a rare genetic disorder caused by inefficient metabolic breakdown of the major inhibitory neurotransmitter, γ-aminobutyric acid (GABA). Pathologic brain accumulation of GABA and γ-hydroxybutyrate (GHB), a neuroactive by-product of GABA catabolism, leads to a multitude of molecular [...] Read more.
Succinic semialdehyde dehydrogenase deficiency (SSADHD) is a rare genetic disorder caused by inefficient metabolic breakdown of the major inhibitory neurotransmitter, γ-aminobutyric acid (GABA). Pathologic brain accumulation of GABA and γ-hydroxybutyrate (GHB), a neuroactive by-product of GABA catabolism, leads to a multitude of molecular abnormalities beginning in early life, culminating in multifaceted clinical presentations including delayed psychomotor development, intellectual disability, hypotonia, and ataxia. Paradoxically, over half of patients with SSADHD also develop epilepsy and face a significant risk of sudden unexpected death in epilepsy (SUDEP). Here, we review some of the relevant molecular mechanisms through which impaired synaptic inhibition, astrocytic malfunctions and myelin defects might contribute to the complex SSADHD phenotype. We also discuss the gaps in knowledge that need to be addressed for the implementation of successful gene and enzyme replacement SSADHD therapies. We conclude with a description of a novel SSADHD mouse model that enables ‘on-demand’ SSADH restoration, allowing proof-of-concept studies to fine-tune SSADH restoration in preparation for eventual human trials. Full article
(This article belongs to the Special Issue Molecular Mechanism in Movement Disorders and Neurotransmitter Diseases)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-2
Back to TopTop