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Novel Therapeutic Approaches in Neuroscience Research
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Novel Therapeutic Approaches in Neuroscience Research

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 2023) | Viewed by 14874

Special Issue Editors

Prof. Dr. Marucia Chacur

E-Mail Website
Guest Editor
Laboratory of Functional Neuroanatomy of Pain, Instituto de Ciências Biomédicas, Universidade de Sao Paulo, Sao Paulo 05508-900, SP, Brazil
Interests: analgesic; inflammation; neurotransmitters; non-pharmacological therapies; glial cell; muscle pain; diabetes
Special Issues, Collections and Topics in MDPI journals
Dr. Anne M. Landau

E-Mail Website1 Website2
Guest Editor
1. Translational Neuropsychiatry Unit, Aarhus University, Aarhus, Denmark
2. Department of Nuclear Medicine and PET, Aarhus University Hospital, Aarhus, Denmark
Interests: positron emission tomography (PET); neurodegenerative disorders; putative therapeutics
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Neuroscience is the scientific study of the peripheral and central nervous systems. The aim is to elucidate mechanisms that could better explain disease development and progression in neurological, neurodegenerative and psychiatric illnesses as well as assist in the development of novel therapies. The initial trials and validation of novel therapies in neuroscience research often depend on the use of animal models. Although no animal model is perfect, neuroscience researchers aim to use models which recapitulate key features of the disease under investigation.

The purpose of this Special Issue: “Novel Therapeutic Approaches in Neuroscience Research” is to showcase the use of animal models in neuroscience research and their importance in the trialling of novel therapies. We aim to gather publications detailing the latest progress in the development and evaluation of treatments for neurodegenerative diseases, psychiatric illnesses and pain-related disorders. For this, we are inviting submissions of original research, review articles and perspectives focusing on the molecular mechanisms of pharmacological and non-pharmacological therapies in preclinical neuroscience research.

Prof. Dr. Marucia Chacur
Dr. Anne M. Landau
Guest Editors

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

  • animal models
  • neuroprotection
  • antidepressants
  • analgesia
  • neurodegenerative disease
  • psychi-atric illness
  • pain
  • ageing
  • neurotransmitter
  • glial cells

Published Papers (4 papers)

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Research

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16 pages, 2511 KiB  
Article
Crotalphine Modulates Microglia M1/M2 Phenotypes and Induces Spinal Analgesia Mediated by Opioid-Cannabinoid Systems
by Flavia S. R. Lopes, Aline C. Giardini, Morena B. Sant’Anna, Louise F. Kimura, Michelle C. Bufalo, Hugo Vigerelli, Vanessa O. Zambelli and Gisele Picolo
Int. J. Mol. Sci. 2022, 23(19), 11571; https://doi.org/10.3390/ijms231911571 - 30 Sep 2022
Cited by 5 | Viewed by 2385
Abstract
Pain is a worldwide public health problem and its treatment is still a challenge since clinically available drugs do not completely reverse chronic painful states or induce undesirable effects. Crotalphine is a 14 amino acids synthetic peptide that induces a potent and long-lasting [...] Read more.
Pain is a worldwide public health problem and its treatment is still a challenge since clinically available drugs do not completely reverse chronic painful states or induce undesirable effects. Crotalphine is a 14 amino acids synthetic peptide that induces a potent and long-lasting analgesic effect on acute and chronic pain models, peripherally mediated by the endogenous release of dynorphin A and the desensitization of the transient receptor potential ankyrin 1 (TRPA1) receptor. However, the effects of crotalphine on the central nervous system (CNS) and the signaling pathway have not been investigated. Thus, the central effect of crotalphine was evaluated on the partial sciatic nerve ligation (PSNL)-induced chronic neuropathic pain model. Crotalphine (100 µg/kg, p.o.)-induced analgesia on the 14th day after surgery lasting up to 24 h after administration. This effect was prevented by intrathecal administration of CB1 (AM251) or CB2 (AM630) cannabinoid receptor antagonists. Besides that, crotalphine-induced analgesia was reversed by CTOP, nor-BNI, and naltrindole, antagonists of mu, kappa, and delta-opioid receptors, respectively, and also by the specific antibodies for β-endorphin, dynorphin-A, and met-enkephalin. Likewise, the analgesic effect of crotalphine was blocked by the intrathecal administration of minocycline, an inhibitor of microglial activation and proliferation. Additionally, crotalphine decreased the PSNL-induced IL-6 release in the spinal cord. Importantly, in vitro, crotalphine inhibited LPS-induced CD86 expression and upregulated CD206 expression in BV-2 cells, demonstrating a polarization of microglial cells towards the M2 phenotype. These results demonstrated that crotalphine, besides activating opioid and cannabinoid analgesic systems, impairs central neuroinflammation, confirming the neuromodulatory mechanism involved in the crotalphine analgesic effect. Full article
(This article belongs to the Special Issue Novel Therapeutic Approaches in Neuroscience Research)
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20 pages, 3738 KiB  
Article
Dual Mechanism of Action of Curcumin in Experimental Models of Multiple Sclerosis
by Ines ELBini-Dhouib, Maroua Manai, Nour-elhouda Neili, Soumaya Marzouki, Ghada Sahraoui, Warda Ben Achour, Sondes Zouaghi, Melika BenAhmed, Raoudha Doghri and Najet Srairi-Abid
Int. J. Mol. Sci. 2022, 23(15), 8658; https://doi.org/10.3390/ijms23158658 - 4 Aug 2022
Cited by 14 | Viewed by 2576
Abstract
Background: Multiple sclerosis (MS) is characterized by a combination of inflammatory and demyelination processes in the spinal cord and brain. Conventional drugs generally target the autoimmune response, without any curative effect. For that reason, there is a great interest in identifying novel agents [...] Read more.
Background: Multiple sclerosis (MS) is characterized by a combination of inflammatory and demyelination processes in the spinal cord and brain. Conventional drugs generally target the autoimmune response, without any curative effect. For that reason, there is a great interest in identifying novel agents with anti-inflammatory and myelinating effects, to counter the inflammation and cell death distinctive of the disease. Methods and results: An in vitro assay showed that curcumin (Cur) at 10 µM enhanced the proliferation of C8-D1A cells and modulated the production of Th1/Th2/Th17 cytokines in the cells stimulated by LPS. Furthermore, two in vivo pathophysiological experimental models were used to assess the effect of curcumin (100 mg/kg). The cuprizone model mimics the de/re-myelination aspect in MS, and the experimental autoimmune encephalomyelitis model (EAE) reflects immune-mediated events. We found that Cur alleviated the neurological symptomatology in EAE and modulated the expression of lymphocytes CD3 and CD4 in the spinal cord. Interestingly, Cur restored motor and behavioral deficiencies, as well as myelination, in demyelinated mice, as indicated by the higher index of luxol fast blue (LFB) and the myelin basic protein (MBP) intensity in the corpus callosum. Conclusions: Curcumin is a potential therapeutic agent that can diminish the MS neuroimmune imbalance and demyelination through its anti-inflammatory and antioxidant effects. Full article
(This article belongs to the Special Issue Novel Therapeutic Approaches in Neuroscience Research)
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Review

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12 pages, 909 KiB  
Review
A2A Adenosine Receptor: A Possible Therapeutic Target for Alzheimer’s Disease by Regulating NLRP3 Inflammasome Activity?
by Stefania Merighi, Manuela Nigro, Alessia Travagli, Silvia Pasquini, Pier Andrea Borea, Katia Varani, Fabrizio Vincenzi and Stefania Gessi
Int. J. Mol. Sci. 2022, 23(9), 5056; https://doi.org/10.3390/ijms23095056 - 2 May 2022
Cited by 10 | Viewed by 3046
Abstract
The A2A adenosine receptor, a member of the P1 purinergic receptor family, plays a crucial role in the pathophysiology of different neurodegenerative illnesses, including Alzheimer’s disease (AD). It regulates both neurons and glial cells, thus modulating synaptic transmission and neuroinflammation. AD is [...] Read more.
The A2A adenosine receptor, a member of the P1 purinergic receptor family, plays a crucial role in the pathophysiology of different neurodegenerative illnesses, including Alzheimer’s disease (AD). It regulates both neurons and glial cells, thus modulating synaptic transmission and neuroinflammation. AD is a complex, progressive neurological condition that is the leading cause of dementia in the world’s old population (>65 years of age). Amyloid peptide-β extracellular accumulation and neurofibrillary tangles constitute the principal etiologic tracts, resulting in apoptosis, brain shrinkage, and neuroinflammation. Interestingly, a growing body of evidence suggests a role of NLRP3 inflammasome as a target to treat neurodegenerative diseases. It represents a tripartite multiprotein complex including NLRP3, ASC, and procaspase-1. Its activation requires two steps that lead with IL-1β and IL-18 release through caspase-1 activation. NLRP3 inhibition provides neuroprotection, and in recent years adenosine, through the A2A receptor, has been reported to modulate NLRP3 functions to reduce organ damage. In this review, we describe the role of NLRP3 in AD pathogenesis, both alone and in connection to A2A receptor regulation, in order to highlight a novel approach to address treatment of AD. Full article
(This article belongs to the Special Issue Novel Therapeutic Approaches in Neuroscience Research)
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32 pages, 1448 KiB  
Review
MicroRNA Alteration, Application as Biomarkers, and Therapeutic Approaches in Neurodegenerative Diseases
by T. P. Nhung Nguyen, Mandeep Kumar, Ernesto Fedele, Giambattista Bonanno and Tiziana Bonifacino
Int. J. Mol. Sci. 2022, 23(9), 4718; https://doi.org/10.3390/ijms23094718 - 25 Apr 2022
Cited by 33 | Viewed by 6087
Abstract
MicroRNAs (miRNAs) are essential post-transcriptional gene regulators involved in various neuronal and non-neuronal cell functions and play a key role in pathological conditions. Numerous studies have demonstrated that miRNAs are dysregulated in major neurodegenerative diseases, such as Alzheimer’s disease, Parkinson’s disease, multiple sclerosis, [...] Read more.
MicroRNAs (miRNAs) are essential post-transcriptional gene regulators involved in various neuronal and non-neuronal cell functions and play a key role in pathological conditions. Numerous studies have demonstrated that miRNAs are dysregulated in major neurodegenerative diseases, such as Alzheimer’s disease, Parkinson’s disease, multiple sclerosis, amyotrophic lateral sclerosis, or Huntington’s disease. Hence, in the present work, we constructed a comprehensive overview of individual microRNA alterations in various models of the above neurodegenerative diseases. We also provided evidence of miRNAs as promising biomarkers for prognostic and diagnostic approaches. In addition, we summarized data from the literature about miRNA-based therapeutic applications via inhibiting or promoting miRNA expression. We finally identified the overlapping miRNA signature across the diseases, including miR-128, miR-140-5p, miR-206, miR-326, and miR-155, associated with multiple etiological cellular mechanisms. However, it remains to be established whether and to what extent miRNA-based therapies could be safely exploited in the future as effective symptomatic or disease-modifying approaches in the different human neurodegenerative disorders. Full article
(This article belongs to the Special Issue Novel Therapeutic Approaches in Neuroscience Research)
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