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Recent Advances in Neuroprotective Drug Development and Therapeutic Applications

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Prof. Dr. Jolanta Helena Kotlińska

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Department of Pharmacology and Pharmacodynamics, Medical University of Lublin, Chodźki 4a St., 20-093 Lublin, Poland
Interests: experimental neuropharmacology and neuroprotective drug development; molecular mechanisms of neuroprotection; dopaminergic; glutamatergic; endocannabinoid signaling in neurodevelopmental and stress-related disorders; animal models of early-life stress and trauma

Special Issue Information

Dear Colleagues,

Neurodevelopmental and stress-related disorders constitute a growing challenge for modern medicine, with limited therapeutic options capable of effectively preventing or reversing central nervous system dysfunction. In this context, neuroprotective drug development has emerged as a promising strategy to preserve neuronal integrity and improve functional outcomes.

This Special Issue, “Recent Advances in Neuroprotective Drug Development and Therapeutic Applications”, aims to highlight recent progress in experimental and translational neuropharmacology, with particular emphasis on molecular and cellular mechanisms underlying neuroprotection. We welcome original research articles and reviews addressing neuroprotective strategies targeting dopaminergic, glutamatergic, and endocannabinoid signaling, synaptic plasticity, and stress-related neuroadaptations.

Both basic and translational studies employing validated experimental models are encouraged, with the goal of advancing neuroprotective drug development and therapeutic applications in central nervous system disorders.

MSc Justyna Lublińska is a doctoral student under the supervision of Prof. Jolanta Kotlińska and will assist in the management of this Special Issue.

Prof. Dr. Jolanta Helena Kotlińska
Guest Editor

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Research

19 pages, 7842 KB

Open AccessArticle

Mitochondrial Homeostasis Mediates the Sustained Neuroprotection of CNTF-Chitosan Hydrogel Against NMDA-Induced Retinal Ganglion Cell Excitotoxicity

by Huiting Jiang, Xunhui Guo, Yuanyuan Bai, Xinyue Ma, Hongmei Duan, Xiaoguang Li and Zhaoyang Yang

Int. J. Mol. Sci. 2026, 27(16), 7200; https://doi.org/10.3390/ijms27167200 - 12 Aug 2026

Viewed by 312

Abstract

N-methyl-D-aspartate (NMDA) excitotoxicity drives mitochondrial dysfunction and retinal ganglion cell (RGC) loss in blinding retinal disorders. Ciliary neurotrophic factor (CNTF) is neuroprotective, but its short half-life limits long-term therapy. Here, we investigated whether mitochondrial homeostasis mediates the sustained protection of a CNTF-loaded chitosan hydrogel. In vitro, free CNTF and the hydrogel equally protected RGCs against NMDA, effects completely abolished by the mitochondrial uncoupler carbonyl cyanide m-chlorophenyl hydrazone (CCCP). In vivo, free CNTF provided only transient rescue, whereas the hydrogel sustained RGC survival, mitochondrial integrity, and visual function for 28 days, with persistent upregulation of mitochondrial biogenesis genes. Adeno-associated virus-mediated DRP1 overexpression-induced mitochondrial fission fully reversed the hydrogel’s benefits, mirroring CCCP inhibition. Collectively, intact mitochondrial homeostasis is essential for the long-term neuroprotection of the CNTF-chitosan hydrogel, which extends CNTF retention without altering its mitochondrial-dependent mechanism. This hydrogel represents a promising long-acting treatment for retinal excitotoxicity. Full article

(This article belongs to the Special Issue Recent Advances in Neuroprotective Drug Development and Therapeutic Applications)

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24 pages, 30525 KB

Open AccessArticle

ATF3/SLC31A1-Mediated Cuproptosis Contributes to Bortezomib-Induced Peripheral Neurotoxicity and Intervention by (−)-Epigallocatechin Gallate

by Yonghai Wang, Jiabin Lu, Xuejing Feng, Bo Yang, Qiaojun He, Peihua Luo and Xiaochun Yang

Int. J. Mol. Sci. 2026, 27(8), 3680; https://doi.org/10.3390/ijms27083680 - 21 Apr 2026

Cited by 1 | Viewed by 864

Abstract

Bortezomib (BTZ), the first-generation proteasome inhibitor, has been approved for the treatment of relapsed, refractory, and newly diagnosed multiple myeloma. Despite its remarkable antitumor efficacy, BTZ treatment is severely limited by a high incidence of systemic adverse reactions, primarily due to its non-selective cytotoxicity toward rapidly dividing normal cells and its potent neurotoxic effects on peripheral neurons. Bortezomib-induced peripheral neurotoxicity (BIPN) manifests as neuropathic pain and sensory abnormalities, affecting up to 31% to 64% of patients and limiting BTZ’s clinical use. Currently, the underlying mechanisms of BIPN are poorly understood. To evaluate the effects of BTZ on the functions of peripheral nerves in mice, we administered an intraperitoneal injection treatment for four weeks. Results indicated that BIPN caused mechanical allodynia, gait abnormalities, and pathological changes in myelin and axons in mice. This study confirms that BTZ upregulates the expression of the activating transcription factor 3 (ATF3), which in turn mediates the increased expression of the copper transporter SLC31A1, causing dysregulation of intracellular copper ion homeostasis and subsequent copper accumulation, and ultimately inducing the development of peripheral neurotoxicity. Elevated intracellular copper concentration exerts a dual effect: it directly promotes the oligomerization of Dihydrolipoamide S-acetyltransferase (DLAT) and concurrently damages the iron–sulfur cluster protein ferredoxin 1 (FDX1), collectively triggering the onset of cuproptosis. Green tea has garnered attention for its rich content of catechins, with (−)-Epigallocatechin Gallate (EGCG) being the most abundant catechin present. This study uncovers the molecular mechanism by which EGCG inhibits BTZ-induced cuproptosis through targeted regulation of copper homeostasis. Analyses demonstrate that EGCG significantly downregulates the expression of the copper transporter SLC31A1, thereby effectively suppressing transmembrane influx of extracellular copper ions. This intervention markedly reduces intracellular copper overload, eliciting a dual regulatory effect: on one hand, the decreased copper concentration directly inhibits the oligomerization of DLAT; on the other hand, it effectively protects the iron–sulfur cluster protein FDX1 from damage. This study aims to systematically elucidate the molecular mechanisms underlying BIPN and to evaluate the therapeutic potential of EGCG in alleviating BIPN, offering a novel therapeutic strategy for the prevention and treatment of BIPN. Full article

(This article belongs to the Special Issue Recent Advances in Neuroprotective Drug Development and Therapeutic Applications)

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