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Biomolecules
Special Issues
New Discoveries in the Field of Neuropharmacology
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New Discoveries in the Field of Neuropharmacology

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: 31 March 2026 | Viewed by 3340

Special Issue Editors

Dr. Beatrice Mihaela Radu

E-Mail Website
Guest Editor
Department of Anatomy, Animal Physiology and Biophysics, Faculty of Biology, University of Bucharest, Splaiul Independentei 91-95, 050095 Bucharest, Romania
Interests: blood–brain barrier; drug safety; drug arrhythmogenic effects; neuropharmacology; epileptogenesis; depression
Special Issues, Collections and Topics in MDPI journals
Dr. Bogdan Amuzescu

E-Mail Website
Guest Editor
Department of Anatomy, Animal Physiology and Biophysics, Faculty of Biology, University of Bucharest, 050095 Bucharest, Romania
Interests: biophysical and pharmacological properties of ion channels (particularly ENaC/Deg and TRP channels); mathematical modeling of complex biological systems; applied research in cardiac electrophysiology and cardiac safety drug testing; stem cells – diagnostic and therapeutic applications

Special Issue Information

Dear Colleagues,

This is an inspiring time in biomedical sciences, where new, dynamic methods are being developed and used to produce groundbreaking results in fundamental and applied research, including neuroscience and related fields, such as neuropharmacology. Every year, new promising drugs (new molecular entities) are approved and launched on the market, offering hope to numerous patients affected by severe and debilitating neurologic and psychiatric disorders. This outcome is the result of the systematic application of advanced and highly effective techniques along the different stages of drug R&D pipelines, starting with in silico methods, new in vitro assays, high-throughput screening approaches, animal models of disease, wide genome sequencing and gene expression techniques, powerful transfection vectors, gene editing, stem cells, and many other marvels of modern science. To reflect this extensive progress in neuropharmacology research, we are launching a Special Issue in the prestigious and highly dynamic Biomolecules journal. Therefore, as guest editors, we warmly invite you to contribute by submitting manuscripts containing some of your recent original research results or comprehensive review studies on this topic. We aim to expedite a fair evaluation in this open-access publication of selected papers, offering good scientific visibility.

Yours sincerely,

Dr. Beatrice Mihaela Radu
Dr. Bogdan Amuzescu
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 250 words) can be sent to the Editorial Office for assessment.

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. Biomolecules 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 2700 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

  • neurologic and psychiatric diseases pharmacology
  • in silico drug screening
  • in vitro pharmacology assays
  • animal models
  • neuropharmacogenomics
  • drug safety
  • blood brain barrier
  • electrophysiology
  • patch-clamp

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Published Papers (2 papers)

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Research

15 pages, 4357 KB  
Article
Assessment of [125I]a-Bungarotoxin Binding to a7 Nicotinic Acetylcholinergic Receptors in Hippocampus-Subiculum of Postmortem Human Parkinson’s Disease Brain
by Fariha Karim, Allyson Ngo, Titus E. Tucker, Ashlee D. L. Coronel and Jogeshwar Mukherjee
Biomolecules 2025, 15(12), 1686; https://doi.org/10.3390/biom15121686 - 2 Dec 2025
Viewed by 406
Abstract
Parkinson’s disease (PD) involves motor and cognitive impairment that nicotinic acetylcholine receptors (nAChRs) such as the α7 subtype are responsible for regulating. The hippocampus, abundant in α7 nAChRs, was quantitatively evaluated for [125I]α-bungarotoxin ([125I]α-Bgtx) binding to α7 nAChRs in [...] Read more.
Parkinson’s disease (PD) involves motor and cognitive impairment that nicotinic acetylcholine receptors (nAChRs) such as the α7 subtype are responsible for regulating. The hippocampus, abundant in α7 nAChRs, was quantitatively evaluated for [125I]α-bungarotoxin ([125I]α-Bgtx) binding to α7 nAChRs in postmortem human PD (n = 26; 12 male, 14 female) and cognitively normal (CN) (n = 29; 14 male, 15 female) brain slices. Anti-ubiquitin and anti-α-synuclein immunostained adjacent slices were analyzed using QuPath. Autoradiographs of [125I]α-Bgtx radioligand binding were analyzed in OptiQuant. Ubiquitin and α-synuclein distribution generally aligned with the distribution of α7 nAChRs detected by [125I]α-Bgtx. Binding of [125I]α-Bgtx in PD cases was significantly greater than CN with a 32% increase in gray matter binding. A weak positive correlation between age and [125I]α-Bgtx binding was found in both PD and CN. In comparison to Alzheimer’s disease hippocampus, [125I]α-Bgtx binding in PD gray matter was higher by 41%. Differences in nAChR expression imply unique roles depending on the neurodegenerative pathology. PD may experience an increase in α7 nAChRs as a compensatory mechanism to the loss in neurons, highlighting its neuroprotective capabilities. [125I]α-Bgtx shows potential as a radioligand for α7 nAChRs to elucidate the complexities of PD pathology. Full article
(This article belongs to the Special Issue New Discoveries in the Field of Neuropharmacology)
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19 pages, 6004 KB  
Article
Inhibitory Effects of Cenobamate on Multiple Human Cardiac Ion Channels and Possible Arrhythmogenic Consequences
by Andreea Larisa Mateias, Florian Armasescu, Bogdan Amuzescu, Alexandru Dan Corlan and Beatrice Mihaela Radu
Biomolecules 2024, 14(12), 1582; https://doi.org/10.3390/biom14121582 - 11 Dec 2024
Cited by 2 | Viewed by 2293
Abstract
Cenobamate is a novel third-generation antiepileptic drug used for the treatment of focal onset seizures and particularly for multi-drug-resistant epilepsy; it acts on multiple targets: GABAA receptors (EC50 42–194 µM) and persistent neuronal Na+ currents (IC50 59 µM). Side [...] Read more.
Cenobamate is a novel third-generation antiepileptic drug used for the treatment of focal onset seizures and particularly for multi-drug-resistant epilepsy; it acts on multiple targets: GABAA receptors (EC50 42–194 µM) and persistent neuronal Na+ currents (IC50 59 µM). Side effects include QTc interval shortening with >20 ms, but not <300 ms. Our in vitro cardiac safety pharmacology study was performed via whole-cell patch-clamp on HEK293T cells with persistent/inducible expression of human cardiac ion channel isoforms hNav1.5 (INa), hCav1.2 (α1c + β2 + α2δ1) (ICaL), hKv7.1 + minK (IKs), and hKv11.1 (hERG) (IKr). We found IC50 of 87.6 µM (peak INa), 46.5 µM (late INa), and 509.75 µM (ICaL). In experiments on Ncyte® ventricular cardiomyocytes, APD90 was reduced with 28.6 ± 13.5% (mean ± SD) by cenobamate 200 µM. Cenobamate’s marked inhibition of INa raises the theoretical possibility of cardiac arrhythmia induction at therapeutic concentrations in the context of preexisting myocardial pathology, in the presence of action potential conduction and repolarization heterogeneity. This hypothetical mechanism is consistent with the known effects of class Ib antiarrhythmics. In simulations with a linear strand of 50 cardiomyocytes with variable inter-myocyte conductance based on a modified O’Hara–Rudy model, we found a negligible cenobamate-induced conduction delay in normal tissue, but a marked delay and also a block when gap junction conduction was already depressed. Full article
(This article belongs to the Special Issue New Discoveries in the Field of Neuropharmacology)
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