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Therapeutic Agents for Neurological Disorders, 3rd Edition
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Therapeutic Agents for Neurological Disorders, 3rd Edition

A special issue of Pharmaceuticals (ISSN 1424-8247). This special issue belongs to the section "Pharmacology".

Deadline for manuscript submissions: closed (30 June 2024) | Viewed by 12866

Special Issue Editor

Dr. Damian Holsinger

E-Mail Website
Guest Editor
Neuroscience, School of Medical Sciences, Faculty of Medicine and Health, The University of Sydney, Camperdown, NSW 2006, Australia
Interests: neurodegenerative diseases; Alzheimer’s disease; dementia; cell biology; molecular biology; ageing; therapeutics
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Neurological disorders are disabling conditions that encompass, but are not limited to, cerebrovascular diseases, epilepsy, dementias (Alzheimer’s, frontotemporal and others), multiple sclerosis, movement disorders (Parkinson’s, amyotrophic lateral sclerosis and others), brain tumors and neuroinfections, amongst others. Globally, neurological disorders are the leading cause of disability-adjusted life years (DALYs). The absolute number of deaths and DALYs from all neurological disorders combined has increased significantly in the last decade. These findings outline an impending epidemic that requires urgent attention. Treatments for neurological disorders are challenging, but numerous advancements have been made in identifying mechanisms and delineating the pathways underlying these diseases. Advances in technologies that garner information from the fields of bioinformatics and next-generation and whole-genome sequencing have added invaluable support in identifying "culprit" genes and proteins. Using this information, scientists and clinicians have ventured into areas previously deemed "fiction". From brain-controlled, non-invasive muscle stimulators that help paraplegics walk to the editing of the CEP290 gene in individuals with Leber congenital amaurosis 10 (LCA10) and a plethora of therapies in between, biomedicine has made giant leaps in just over two decades. 

This Special Issue aims to draw together research from experts in the field that highlight therapeutic agents and strategies and identify future directions that will lead to discoveries and therapies for neurological disorders.

Dr. Damian Holsinger
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. Pharmaceuticals 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 2900 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

  • neurodegeneration
  • brain injury
  • spinal cord injury
  • neurodevelopmental disorders
  • nerve repair
  • brain tumors
  • neuromodulation
  • neuroinflammation

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Related Special Issues

Published Papers (3 papers)

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Research

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18 pages, 3559 KiB  
Article
Canagliflozin Ameliorates Oxidative Stress and Autistic-like Features in Valproic-Acid-Induced Autism in Rats: Comparison with Aripiprazole Action
by Mohammed Moutaz Nakhal, Petrilla Jayaprakash, Salahdein Aburuz, Bassem Sadek and Amal Akour
Pharmaceuticals 2023, 16(5), 769; https://doi.org/10.3390/ph16050769 - 19 May 2023
Cited by 13 | Viewed by 2772
Abstract
Based on their proven anti-inflammatory and antioxidant effects, recent studies have examined the therapeutic potential of the sodium-glucose cotransporter 2 (SGLT2) inhibitors in neurodevelopmental disorders such as autism spectrum disorder (ASD). Therefore, the aim of this study is to assess the effects of [...] Read more.
Based on their proven anti-inflammatory and antioxidant effects, recent studies have examined the therapeutic potential of the sodium-glucose cotransporter 2 (SGLT2) inhibitors in neurodevelopmental disorders such as autism spectrum disorder (ASD). Therefore, the aim of this study is to assess the effects of subchronic systemic treatment with intraperitoneal (i.p.) canagliflozin (20, 50, and 100 mg/kg) compared to aripiprazole (ARP) (3 mg/g, i.p.) in a valproic acid (VPA)-induced rat model of autism. The behavioral characteristics of ASD, oxidative stress, and acetylcholinesterase (AChE) activity in rats with ASD-like behaviors, which were induced by prenatal exposure to VPA, were evaluated. The behavioral assessment methods used for this study were the open field test (OFT), the marble-burying test (MBT), and the nestlet-shredding test (NST) to examine their exploratory, anxiety, and compulsiveness-like actions, while the biochemical assessment used for this study was an ELISA colorimetric assay to measure ASD biomarker activity in the hippocampus, prefrontal cortex, and cerebellum. Rats that were pretreated with 100 mg/kg of canagliflozin displayed a significantly lower percentage of shredding (1.12 ± 0.6%, p < 0.01) compared to the ARP group (3.52 ± 1.6%). Pretreatment with (20 mg/kg, 50 mg/kg, and 100 mg/kg) canagliflozin reversed anxiety levels and hyperactivity and reduced hyper-locomotor activity significantly (161 ± 34.9 s, p < 0.05; 154 ± 44.7 s, p < 0.05; 147 ± 33.6 s, p < 0.05) when compared with the VPA group (303 ± 140 s). Moreover, canagliflozin and ARP mitigated oxidative stress status by restoring levels of glutathione (GSH) and catalase (CAT) and increasing the levels of malondialdehyde (MDA) in all tested brain regions. The observed results propose repurposing of canagliflozin in the therapeutic management of ASD. However, further investigations are still required to verify the clinical relevance of canagliflozin in ASD. Full article
(This article belongs to the Special Issue Therapeutic Agents for Neurological Disorders, 3rd Edition)
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Review

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15 pages, 275 KiB  
Review
Towards Treating Multiple Sclerosis Progression
by Darius Häusler and Martin S. Weber
Pharmaceuticals 2024, 17(11), 1474; https://doi.org/10.3390/ph17111474 - 2 Nov 2024
Viewed by 2204
Abstract
Multiple sclerosis (MS) is an inflammatory, demyelinating disease of the central nervous system (CNS). In most patients, the disease starts with an acute onset followed by a remission phase, subsequent relapses and a later transition to steady chronic progression. In a minority of [...] Read more.
Multiple sclerosis (MS) is an inflammatory, demyelinating disease of the central nervous system (CNS). In most patients, the disease starts with an acute onset followed by a remission phase, subsequent relapses and a later transition to steady chronic progression. In a minority of patients, this progressive phase develops from the beginning. MS relapses are characterized predominantly by the de novo formation of an inflammatory CNS lesion and the infiltration of immune cells, whereas the pathological features of MS progression include slowly expanding lesions, global brain atrophy and an inflammatory response predominantly mediated by macrophages/microglia. Importantly, this CNS-intrinsic pathophysiology appears to initiate early during the relapsing–remitting disease phase, while it turns into the key clinical MS feature in later stages. Currently approved disease-modifying treatments for MS are effective in modulating peripheral immunity by dampening immune cell activity or preventing the migration of immune cells into the CNS, resulting in the prevention of relapses; however, they show limited success in halting MS progression. In this manuscript, we first describe the pathological mechanisms of MS and summarize the approved therapeutics for MS progression. We also review the treatment options for progressive MS (PMS) that are currently under investigation. Finally, we discuss potential targets for novel treatment strategies in PMS. Full article
(This article belongs to the Special Issue Therapeutic Agents for Neurological Disorders, 3rd Edition)

Other

Jump to: Research, Review

14 pages, 1628 KiB  
Systematic Review
Effect of Botulinum Toxin Injections in the Treatment of Spasticity of Different Etiologies: An Umbrella Review
by Iris Otero-Luis, Arturo Martinez-Rodrigo, Iván Cavero-Redondo, Nerea Moreno-Herráiz, Irene Martínez-García and Alicia Saz-Lara
Pharmaceuticals 2024, 17(3), 310; https://doi.org/10.3390/ph17030310 - 28 Feb 2024
Cited by 4 | Viewed by 7081
Abstract
Background: Spasticity is a very common neurological sequelae that significantly impacts the quality of life of patients, affecting more than 12 million people worldwide. Botulinum toxin is considered a reversible treatment for spasticity, but due to the large amount of available evidence, synthesis [...] Read more.
Background: Spasticity is a very common neurological sequelae that significantly impacts the quality of life of patients, affecting more than 12 million people worldwide. Botulinum toxin is considered a reversible treatment for spasticity, but due to the large amount of available evidence, synthesis seems necessary. Therefore, we conducted an overview of existing systematic reviews and meta-analyses to evaluate the effect of botulinum toxin injections in the treatment of spasticity of different etiologies. Methods: A systematic search of different databases, including Pubmed, Scopus, the Cochrane Library, and Web of Science, was performed from inception to February 2024. Standardized mean differences (SMDs) and their respective 95% confidence intervals (CIs) were calculated to assess the effect of botulinum toxin compared to that of the control treatment using the Modified Ashworth Scale (MAS). All the statistical analyses were performed using STATA 15 software. Results: 28 studies were included in the umbrella review. The effect of botulinum toxin injections on spasticity, as measured by the MAS, was significantly lower in all but three studies, although these studies also supported the intervention. The SMDs reported by the meta-analyses ranged from −0.98 to −0.01. Conclusion: Botulinum toxin injections were effective at treating spasticity of different etiologies, as indicated by the measurements on the MAS. This implies an improvement in muscle tone and, consequently, in the patient’s mobility and quality of life. Full article
(This article belongs to the Special Issue Therapeutic Agents for Neurological Disorders, 3rd Edition)
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