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Pharmaceuticals
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Therapeutics Agents for Neural Repair 2023
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Therapeutics Agents for Neural Repair 2023

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

Deadline for manuscript submissions: closed (31 December 2023) | Viewed by 6461

Special Issue Editor

Dr. Nuno Silva

E-Mail Website
Guest Editor
Life and Health Sciences Research Institute (ICVS), School of Medicine, University of Minho, Campus de Gualtar, 4710-057 Braga, Portugal
Interests: spinal cord injury; biomaterials; pharmacology; regeneration; immunomodulation
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

An insult to the central nervous system (CNS) usually leads to permanent and irreversible pathological conditions. Events such as stroke, trauma, or neurodegenerative diseases have a strong impact on the physiological, psychological, and social behaviors of patients. For these reasons, it is urgent to develop therapeutic strategies that can specifically target these problems. Typically, the pathophysiology of these conditions entails several molecular as well as cellular events and, given its multifaceted nature, many conceptually different paths are under investigation to promote neural repair. This Special Issue is dedicated to “Therapeutic Agents for Neural Repair”, and it is mainly focused on the use of pharmaceutical agents administrated alone or in combination with other therapeutic approaches.

I sincerely hope that you will be able to contribute a research manuscript or review article dealing with your research in this area of investigation. The proposed topics include, but are not limited to, the following:

  • Pathologies of the CNS (Parkinson's, Alzheimer’s, Huntington’s, multiple sclerosis, depression, autism, Machado–Joseph, amyotrophic lateral sclerosis, stroke, traumatic brain injury, and spinal cord injury).
  • Therapeutic approaches (molecular therapy, cell therapy, gene therapy, deep brain/epidural stimulation, and tissue engineering).
  • Personalized medicine.
  • Biomarkers of disease.
  • In vitro/ex vivo studies.
  • In vivo preclinical studies.
  • Clinical studies.

I look forward to your participation.

Dr. Nuno A. Silva
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.

Related Special Issues

Published Papers (4 papers)

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Research

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12 pages, 830 KiB  
Article
Sarcosine May Induce EGF Production or Inhibit the Decline in EGF Concentrations in Patients with Chronic Schizophrenia (Results of the PULSAR Study)
by Agnieszka Pawlak, Bartosz Kaczmarek, Adam Wysokiński and Dominik Strzelecki
Pharmaceuticals 2023, 16(11), 1557; https://doi.org/10.3390/ph16111557 - 3 Nov 2023
Viewed by 1040
Abstract
Sarcosine (N-methylglycine), a glutamatergic modulator, reduces the primary negative symptoms of schizophrenia. These beneficial changes might be mediated by trophic factors such as epidermal growth factor (EGF). We assessed associations between initial serum EGF levels or changes in serum EGF levels and symptom [...] Read more.
Sarcosine (N-methylglycine), a glutamatergic modulator, reduces the primary negative symptoms of schizophrenia. These beneficial changes might be mediated by trophic factors such as epidermal growth factor (EGF). We assessed associations between initial serum EGF levels or changes in serum EGF levels and symptom severity during the addition of sarcosine to stable antipsychotic treatment and thereby evaluated the associations between glutamatergic modulation, clinical changes and peripheral EGF concentrations. Fifty-eight subjects with a diagnosis of chronic schizophrenia with dominant negative symptoms, stably treated with antipsychotics, completed a prospective 6-month, randomized, double-blind, placebo-controlled study. Subjects received orally 2 g of sarcosine (n = 28) or placebo (n = 30) daily. Serum EGF levels and symptom severity (using the Positive and Negative Syndrome Scale (PANSS) and the Calgary Depression Scale for Schizophrenia (CDSS)) were assessed at baseline, 6-week and 6-month follow-up. Augmentation antipsychotic treatment with sarcosine had no effect on EGF serum levels at any time points. Only the sarcosine group showed a significant improvement in negative symptoms, general psychopathology subscales and the overall PANSS score. We found a reduction in serum EGF levels in the placebo group, but levels in the sarcosine remained stable during the study. Our data indicate that improvement in negative symptoms due to sarcosine augmentation is not directly mediated by EGF, but effective treatment may induce the production or block the decrease in EGF concentrations, which indicates the neuroprotective effect of treatment and confirms the relationship between neuroprotection and EGF levels. Full article
(This article belongs to the Special Issue Therapeutics Agents for Neural Repair 2023)
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14 pages, 1486 KiB  
Article
Synthetic Thyroid Hormone Receptor-β Agonists Promote Oligodendrocyte Precursor Cell Differentiation in the Presence of Inflammatory Challenges
by Vito Antonio Baldassarro, Corinne Quadalti, Massimiliano Runfola, Clementina Manera, Simona Rapposelli and Laura Calzà
Pharmaceuticals 2023, 16(9), 1207; https://doi.org/10.3390/ph16091207 - 25 Aug 2023
Viewed by 1152
Abstract
Oligodendrocytes and their precursors are the cells responsible for developmental myelination and myelin repair during adulthood. Their differentiation and maturation processes are regulated by a complex molecular machinery driven mainly by triiodothyronine (T3), the genomic active form of thyroid hormone, which binds to [...] Read more.
Oligodendrocytes and their precursors are the cells responsible for developmental myelination and myelin repair during adulthood. Their differentiation and maturation processes are regulated by a complex molecular machinery driven mainly by triiodothyronine (T3), the genomic active form of thyroid hormone, which binds to thyroid hormone receptors (TRs), regulating the expression of target genes. Different molecular tools have been developed to mimic T3 action in an attempt to overcome the myelin repair deficit that underlies various central nervous system pathologies. In this study, we used a well-established in vitro model of neural stem cell-derived oligodendrocyte precursor cells (OPCs) to test the effects of two compounds: the TRβ1 ligand IS25 and its pro-drug TG68. We showed that treatment with TG68 induces OPC differentiation/maturation as well as both the natural ligand and the best-known TRβ1 synthetic ligand, GC-1. We then described that, unlike T3, TG68 can fully overcome the cytokine-mediated oligodendrocyte differentiation block. In conclusion, we showed the ability of a new synthetic compound to stimulate OPC differentiation and overcome inflammation-mediated pathological conditions. Further studies will clarify whether the compound acts as a pro-drug to produce the TRβ1 ligand IS25 or if its action is mediated by secondary mechanisms such as AMPK activation. Full article
(This article belongs to the Special Issue Therapeutics Agents for Neural Repair 2023)
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Review

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17 pages, 779 KiB  
Review
Taming Postoperative Delirium with Dexmedetomidine: A Review of the Therapeutic Agent’s Neuroprotective Effects following Surgery
by Vincent Bargnes III, Brian Oliver, Emily Wang, Seth Greenspan, Zhaosheng Jin, Isaac Yeung and Sergio Bergese
Pharmaceuticals 2023, 16(10), 1453; https://doi.org/10.3390/ph16101453 - 13 Oct 2023
Viewed by 1551
Abstract
Postoperative delirium (POD) represents a perioperative neurocognitive disorder that has dreaded ramifications on a patient’s recovery from surgery. Dexmedetomidine displays multiple mechanisms of neuroprotection to assist in preventing POD as a part of a comprehensive anesthetic care plan. This review will cover dexmedetomidine’s [...] Read more.
Postoperative delirium (POD) represents a perioperative neurocognitive disorder that has dreaded ramifications on a patient’s recovery from surgery. Dexmedetomidine displays multiple mechanisms of neuroprotection to assist in preventing POD as a part of a comprehensive anesthetic care plan. This review will cover dexmedetomidine’s pharmacological overlap with the current etiological theories behind POD along with pre-clinical and clinical studies on POD prevention with dexmedetomidine. While the body of evidence surrounding the use of dexmedetomidine for POD prevention still requires further development, promising evidence exists for the use of dexmedetomidine in select dosing and circumstances to enhance recovery from surgery. Full article
(This article belongs to the Special Issue Therapeutics Agents for Neural Repair 2023)
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Other

Jump to: Research, Review

15 pages, 6016 KiB  
Brief Report
The Effects of a Blood–Brain Barrier Penetrating Erythropoietin in a Mouse Model of Tauopathy
by Joshua Yang, Weijun Ou, Nataraj Jagadeesan, Juste Simanauskaite, Jiahong Sun, Demi Castellanos, David H. Cribbs and Rachita K. Sumbria
Pharmaceuticals 2023, 16(4), 558; https://doi.org/10.3390/ph16040558 - 7 Apr 2023
Viewed by 2201
Abstract
Erythropoietin (EPO), a hematopoietic neurotrophin, is a potential therapeutic for Alzheimer’s disease (AD) but has limited blood–brain barrier (BBB) permeability. EPO fused to a chimeric transferrin receptor monoclonal antibody (cTfRMAb) enters the brain via TfR-mediated transcytosis across the BBB. We previously showed that [...] Read more.
Erythropoietin (EPO), a hematopoietic neurotrophin, is a potential therapeutic for Alzheimer’s disease (AD) but has limited blood–brain barrier (BBB) permeability. EPO fused to a chimeric transferrin receptor monoclonal antibody (cTfRMAb) enters the brain via TfR-mediated transcytosis across the BBB. We previously showed that cTfRMAb-EPO is protective in a mouse model of amyloidosis, but its effects on tauopathy are not known. Given that amyloid and tau pathology are characteristics of AD, the effects of cTfRMAb-EPO were studied in a tauopathy mouse model (PS19). Six-month-old PS19 mice were injected intraperitoneally with either saline (PS19-Saline; n = 9) or cTfRMAb-EPO (PS19-cTfRMAb-EPO, 10 mg/kg; n = 10); every two or three days on alternate weeks for 8 weeks. Age-matched, saline-treated, wildtype littermates (WT-Saline; n = 12) were injected using the same protocol. After 8 weeks, locomotion, hyperactivity, and anxiety were assessed via the open-field test, and brains were harvested and sectioned. Cerebral cortex, hippocampus, amygdala, and entorhinal cortex sections were analyzed for phospho-tau (AT8) and microgliosis (Iba1). Hippocampal cellular density (H&E) was also assessed. PS19-Saline mice were hyperactive and less anxious compared to WT-Saline mice, and these behavioral phenotypes were significantly reduced in the PS19-cTfRMAb-EPO mice compared to the PS19-Saline mice. cTfRMAb-EPO significantly reduced AT8 load by ≥50% in all of the brain regions analyzed and microgliosis in the entorhinal cortex and amygdala compared to the PS19-Saline mice. Hippocampal pyramidal and granule cell layer density did not differ significantly between the PS19-cTfRMAb-EPO and PS19-Saline mice. This proof-of-concept study demonstrates the therapeutic effects of the BBB-penetrating cTfRMAb-EPO in PS19 mice. Full article
(This article belongs to the Special Issue Therapeutics Agents for Neural Repair 2023)
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