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Brain Sciences
Special Issues
Neuropharmacology and Neuroinflammation
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Neuropharmacology and Neuroinflammation

A special issue of Brain Sciences (ISSN 2076-3425). This special issue belongs to the section "Neuropharmacology and Neuropathology".

Deadline for manuscript submissions: closed (31 July 2024) | Viewed by 6174

Special Issue Editors

Prof. Dr. Vasudevan Mani

E-Mail Website
Guest Editor
Department of Pharmacology and Toxicology, College of Pharmacy, Qassim University, Buraydah 51452, Saudi Arabia
Interests: Alzheimer’s disease; dementia; neuroprotective; pharmacology screening; neuroinflammation; CNS; antidiabetic; animal studies
Dr. Minhajul Areen

E-Mail Website
Guest Editor
Department of Medicinal Chemistry and Pharmacognosy, College of Pharmacy, Qassim University, Buraydah, Saudi Arabia
Interests: inflammation; multitargeted ligands; diabetes; drug design; Alzheimer’s disease

Special Issue Information

Dear Colleagues,

Neuropharmacology offers a comprehensive understanding of how drugs interact with specific molecular targets in the nervous system, demonstrating the influence of drugs over neuronal functions at the molecular, cellular, and systemic levels. It adds to the essential knowledge for developing new molecules intended to offer therapeutic benefits to individuals facing diverse psychiatric and neurological conditions. In a focused context, neuroinflammation refers to inflammation in the brain and spinal cord. This phenomenon entails the activation of immune cells within the central nervous system. Microglia and the resident macrophages of the brain are identified as crucial contributors to the initiation and progression of neuroinflammation. Moreover, microglia and astrocytes release pro-inflammatory mediators, including cytokines, chemokines, and reactive oxygen species, thus establishing inflammation. This Special Issue focuses on exploring research that addresses clinical and pre-clinical drug design, as well as organic synthesis aspects of neuroinflammatory alterations in neurological and psychiatric disorders, which includes epilepsy, depression, anxiety, and neurodegenerative diseases like Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis, Huntington’s disease, and multiple sclerosis.

Prof. Dr. Vasudevan Mani
Dr. Minhajul Areen
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. Brain Sciences 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 2200 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

  • neuroinflammation
  • psychiatric conditions
  • neurodegenerative diseases
  • therapeutic targets
  • natural products
  • toxicity issues
  • oxidative stress
  • mitochondrial damage
  • neuronal apoptosis

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Published Papers (2 papers)

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Research

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22 pages, 2244 KiB  
Article
Betahistine’s Neuroprotective Actions against Lipopolysaccharide-Induced Neurotoxicity: Insights from Experimental and Computational Studies
by Vasudevan Mani and Minhajul Arfeen
Brain Sci. 2024, 14(9), 876; https://doi.org/10.3390/brainsci14090876 - 29 Aug 2024
Cited by 2 | Viewed by 1255
Abstract
Histamine H3 receptor (H3R) antagonists, such as betahistine (BHTE), have shown significant potential in treating central nervous system (CNS) disorders due to their neuroprotective properties. This study investigated BHTE’s effects on lipopolysaccharide (LPS)-induced neurotoxicity, which is associated with neuroinflammation and [...] Read more.
Histamine H3 receptor (H3R) antagonists, such as betahistine (BHTE), have shown significant potential in treating central nervous system (CNS) disorders due to their neuroprotective properties. This study investigated BHTE’s effects on lipopolysaccharide (LPS)-induced neurotoxicity, which is associated with neuroinflammation and neurodegeneration. Rats were divided into groups and pre-treated with BHTE (5 or 10 mg/kg, p.o.) for 30 days, followed by LPS administration (1 mg/kg, i.p.) for 4 consecutive days to induce neurotoxicity. LPS exposure resulted in cognitive impairment, as evidenced by performance deficits in maze tests, and a significant reduction in brain acetylcholine (ACh) levels. Additionally, LPS led to increased neuroinflammation, oxidative stress, mitochondrial dysfunction, and apoptosis. Pre-treatment with BHTE effectively counteracted these effects, improving cognitive performance and restoring ACh levels. BHTE significantly reduced LPS-induced increases in pro-inflammatory markers (COX-2, TNF-α, and IL-6) while enhancing anti-inflammatory cytokines (IL-10 and TGF-β1). Furthermore, BHTE improved mitochondrial function by increasing enzyme levels (MRCC-I, II, and IV) and boosted anti-apoptotic (Bcl-2) and antioxidant defenses (GSH and catalase). BHTE also reduced apoptosis markers, including pro-apoptotic protein caspase-3, and oxidative stress marker malondialdehyde (MDA). Molecular modeling studies revealed that BHTE effectively binds to key enzymes involved in neuroinflammation and apoptosis (AChE, COX-2, and caspase-3), with binding free energies between 4 and 5 kcal/mol, interacting with critical residues. These findings underscore BHTE’s multifaceted neuroprotective effects against LPS-induced neurotoxicity, offering potential therapeutic avenues for managing neuroinflammation and related neurodegenerative disorders. Full article
(This article belongs to the Special Issue Neuropharmacology and Neuroinflammation)
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Review

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16 pages, 1144 KiB  
Review
Amyotrophic Lateral Sclerosis in Long-COVID Scenario and the Therapeutic Potential of the Purinergic System in Neuromodulation
by Júlia Leão Batista Simões, Samantha Webler Eichler, Maria Luíza Raitz Siqueira, Geórgia de Carvalho Braga and Margarete Dulce Bagatini
Brain Sci. 2024, 14(2), 180; https://doi.org/10.3390/brainsci14020180 - 16 Feb 2024
Viewed by 4216
Abstract
Amyotrophic lateral sclerosis (ALS) involves the degeneration of motor neurons and debilitating and possibly fatal symptoms. The COVID-19 pandemic directly affected the quality of life of this group, and the SARS-CoV-2 infection accelerated the present neuroinflammatory process. Furthermore, studies indicate that the infection [...] Read more.
Amyotrophic lateral sclerosis (ALS) involves the degeneration of motor neurons and debilitating and possibly fatal symptoms. The COVID-19 pandemic directly affected the quality of life of this group, and the SARS-CoV-2 infection accelerated the present neuroinflammatory process. Furthermore, studies indicate that the infection may have led to the development of the pathology. Thus, the scenario after this pandemic presents “long-lasting COVID” as a disease that affects people who have been infected. From this perspective, studying the pathophysiology behind ALS associated with SARS-CoV-2 infection and possible supporting therapies becomes necessary when we understand the impact on the quality of life of these patients. Thus, the purinergic system was trained to demonstrate how its modulation can add to the treatment, reduce disease progression, and result in better prognoses. From our studies, we highlight the P2X7, P2X4, and A2AR receptors and how their activity can directly influence the ALS pathway. Full article
(This article belongs to the Special Issue Neuropharmacology and Neuroinflammation)
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