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Biomedicines
Special Issues
New Advances in Neuropharmacology
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New Advances in Neuropharmacology

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Drug Discovery, Development and Delivery".

Deadline for manuscript submissions: 30 April 2026 | Viewed by 743

Special Issue Editors

Dr. Yu-Cheng Ho

E-Mail Website
Guest Editor
School of Medicine, College of Medicine, I-Shou University, Kaohsiung City 82445, Taiwan
Interests: neuropsychiatric disorders; neuropharmacology; neural circuits
Special Issues, Collections and Topics in MDPI journals
Dr. Ming Tatt Lee

E-Mail Website
Guest Editor
Faculty of Pharmaceutical Sciences, UCSI University, Kuala Lumpur, Malaysia
Interests: preclinical neuropsychiatric disorders; substance abuse; cognitive impairment; pharmacology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue aims to showcase cutting-edge research in neuropharmacology, focusing on novel therapeutic strategies, molecular mechanisms, and translational innovations for neurological and psychiatric disorders. With rapid advancements in understanding neural circuitry, neuroinflammation, and synaptic plasticity, this field holds immense potential to address unmet clinical needs in conditions such as Parkinson's disease and Alzheimer's disease, psychological disorders, and many others.

We invite original research articles, reviews, and perspectives that explore emerging drug targets, innovative drug delivery systems, biomarker discovery, and the application of AI/ML in drug design. Contributions addressing pharmacogenomics, neuroprotection, and the repurposing of existing therapeutics are particularly encouraged. Submissions should emphasize mechanistic insights, preclinical-to-clinical translation, and implications for precision medicine.

This issue seeks to bridge interdisciplinary gaps, fostering collaboration among neuroscientists, pharmacologists, and clinicians. By highlighting transformative discoveries, we aim to accelerate the development of safer, more effective neurotherapeutics.

Authors are welcome to submit manuscripts aligned with these themes. All submissions will undergo rigorous peer review to ensure scientific rigor and relevance. Join us in advancing the field of neuropharmacology!

Dr. Yu-Cheng Ho
Dr. Ming Tatt Lee
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. Biomedicines 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 2600 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

  • behavioral neuropharmacology
  • molecular neuropharmacology
  • neuropharmacology
  • neurological disorders
  • neurodegenerative diseases

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Further information on MDPI's Special Issue policies can be found here.

Published Papers (1 paper)

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Research

15 pages, 3176 KB  
Article
Quantitative Measures of Time to Loss of 15% Vital Capacity and Survival Extension in Slowly Progressive Amyotrophic Lateral Sclerosis (ALS) Patients Treated with the Immune Regulator NP001 Suggests an Immunopathogenic Subset of ALS
by Namita A. Goyal, Jinsy A. Andrews, Björn E. Oskarsson, Martina H. Wiedau, Edward J. Kasarskis, Bruce D. Forrest, Rongzhen Zhang, Paige M. Bracci, Matthew W. Davis, Ari Azhir and Michael S. McGrath
Biomedicines 2025, 13(12), 3060; https://doi.org/10.3390/biomedicines13123060 - 12 Dec 2025
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Abstract
Background/Objectives: Overall survival in patients with amyotrophic lateral sclerosis (ALS) is linked to the rate of predicted respiratory vital capacity (PVC) loss. The objective of this study was to test whether changes in quantitative PVC measures over time linked to survival would [...] Read more.
Background/Objectives: Overall survival in patients with amyotrophic lateral sclerosis (ALS) is linked to the rate of predicted respiratory vital capacity (PVC) loss. The objective of this study was to test whether changes in quantitative PVC measures over time linked to survival would define an immunopathogenic subset of ALS responsive to NP001, a regulator of innate immunity. Methods: In a retrospective study, data from intent-to-treat (ITT) population of two phase 2 trials of NP001 were evaluated for over time changes in PVC, time-to-event (TTE) loss of 15% PVC and PVC change from baseline, as linked to survival outcomes in patients treated with NP001 vs placebo. Results: Treatment with NP001 was associated with a significantly lower risk compared to placebo in the loss of 15% PVC over six months (p = 0.01; HR = 0.60, 95% CI: 0.39, 0.90). Data from the two trials were subsequently divided by a disease progression rate (DPR) value of 0.50 units of ALSFRS-R score lost per month for analysis of slow vs. rapid disease. In ALS patients with slowly progressive disease (DPR < 0.50), TTE PVC changes from baseline were slowed (p < 0.0005) and overall survival extended significantly (18.5 months) in NP001-treated vs. placebo groups. The rapidly progressive ALS patients (DPR ≥ 0.50) treated with NP001 showed no significant difference in PVC change or survival from the placebo group. Conclusions: These hypothesis-generating observations suggest that inflammation might play a significant role in the loss of respiratory function in a major subset of ALS patients. Full article
(This article belongs to the Special Issue New Advances in Neuropharmacology)
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