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Biomedicines
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Molecular Mechanisms and Novel Therapies for Brain Injury: 2nd Edition
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Molecular Mechanisms and Novel Therapies for Brain Injury: 2nd Edition

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Neurobiology and Clinical Neuroscience".

Deadline for manuscript submissions: 31 January 2026 | Viewed by 4861

Special Issue Editor

Dr. Arjun Sapkota

E-Mail Website
Guest Editor
Neuroscience Lab, San Diego Biomedical Research Institute, San Diego, CA, 92121, USA
Interests: ischemic stroke; multiple sclerosis; vascular dementia; neuroinflammation; hypoxia; vascular remodeling; drug discovery
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Brain injury—whether that be stroke, spinal cord injury, traumatic brain injury, seizure, brain tumors—is the leading cause of death and disability globally. To date, numerous efforts have been made to develop new therapeutics that modulate the pathogenesis of brain injury. Unfortunately, these studies have not led to the successful development and discovery of new drug targets, biomarkers, and therapeutics that tackle brain injury. Therefore, uncovering the molecular mechanisms of injury, recovery, and neuroprotection is important for the development of novel, effective therapies.

This Special Issue aims to collect up-to-date overviews of the current understandings of brain injury, molecular mechanisms, and novel therapies, as well as the possible clinical translations and therapeutic strategies to treat brain injury. We invite authors to submit of original research articles, reviews, and short notes focusing on molecular mechanisms and novel therapies. These should highlight, but are not limited to, molecular or genetic manipulation affecting protective or detrimental outcomes, the mechanisms of action of various pharmacological agents, innovative therapeutic strategies for treatment, and neuroinflammation.

Dr. Arjun Sapkota
Guest Editor

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. 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

  • stroke
  • spinal cord injury
  • traumatic brain injury
  • seizure
  • brain tumors
  • neurodegeneration
  • neuroinflammation
  • blood–brain barrier disruption
  • neuroprotection
  • drug discover
  • mechanism of action
  • target validation

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Related Special Issue

Published Papers (3 papers)

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Research

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13 pages, 1181 KiB  
Article
Three-Month Durability of Bilateral Two-Level Stellate Ganglion Blocks for Traumatic Brain Injury: A Retrospective Analysis
by Sean W. Mulvaney, Sanjay Mahadevan, Roosevelt J. Desronvilles, Jr., Kyle J. Dineen and Kristine L. Rae Olmsted
Biomedicines 2025, 13(7), 1526; https://doi.org/10.3390/biomedicines13071526 - 23 Jun 2025
Viewed by 1442
Abstract
Background/Objectives: The primary aim of the study was to determine if ultrasound-guided, bilateral, two-level stellate ganglion blocks (SGBs), also known as two-level cervical sympathetic chain blocks (2LCSBs), performed on subsequent days, improve symptoms of chronic mild Traumatic Brain Injury (TBI) over a [...] Read more.
Background/Objectives: The primary aim of the study was to determine if ultrasound-guided, bilateral, two-level stellate ganglion blocks (SGBs), also known as two-level cervical sympathetic chain blocks (2LCSBs), performed on subsequent days, improve symptoms of chronic mild Traumatic Brain Injury (TBI) over a three-month period, as assessed by the Neurobehavioral Symptom Inventory (NSI). A secondary objective was to evaluate sex-based differences in outcomes during the same time period. Methods: A retrospective chart review was conducted between January 2024 and February 2025. We identified 41 patients who received bilateral 2LCSB for chronic (at least 3 months) TBI-related neurobehavioral symptoms as determined by NSI scores. NSI scores were collected at baseline, one week, one month, two months, and three months post treatment in 28 males and 13 females. An analysis of NSI scores and NSI-composite sub-scores was conducted to determine sex-based differences and 3-month differences in outcomes for patients receiving bilateral 2LCSB. Results: Of the 41 patients that underwent the bilateral 2LCSB procedure, 35 showed improvement in their NSI scores (85.36%) and 36 reported improvements in NSI sub-scores (87.8%). Across the entire dataset, patients experienced a 48.44% average decrease in total NSI scores from baseline and an average decrease of 43.11% in NSI sub-scores from baseline, indicative of improvements in TBI-specific symptoms. No statistical difference in outcomes was observed between males and females. Conclusions: Bilateral 2LCSB may provide rapid and durable TBI symptom improvement for 3 months, based on NSI scoring. However, additional research is necessary to establish causality. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Novel Therapies for Brain Injury: 2nd Edition)
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19 pages, 1176 KiB  
Article
Temporal Changes in Mitochondria-Centric Excitotoxic Responses Following Severe Penetrating Traumatic Brain Injury
by Hiren R. Modi, Sudeep Musyaju, Anke H. Scultetus and Jignesh D. Pandya
Biomedicines 2025, 13(7), 1520; https://doi.org/10.3390/biomedicines13071520 - 21 Jun 2025
Viewed by 338
Abstract
Background/Objectives: Traumatic brain injury (TBI) remains a significant and urgent medical concern for the US military. TBI triggers excitotoxic responses immediately, involving mitochondrial dysfunction characterized by loss of calcium (Ca2+) cycling, membrane damage and increased cell death. However, a comprehensive understanding [...] Read more.
Background/Objectives: Traumatic brain injury (TBI) remains a significant and urgent medical concern for the US military. TBI triggers excitotoxic responses immediately, involving mitochondrial dysfunction characterized by loss of calcium (Ca2+) cycling, membrane damage and increased cell death. However, a comprehensive understanding of mitochondria-centric excitotoxic responses over time has yet to be fully demonstrated after severe TBI. The current study evaluated mitochondria-centric time course responses between 30 min and 2 weeks (seven time points) after penetrating TBI (pTBI). Methods: Anesthetized adult male Sprague-Dawley rats were subjected to either 10% unilateral pTBI or Sham craniectomy. Animals were euthanized at various time points, and mitochondria were isolated from the injury core. Results: Post-injury mitochondrial Ca2+ homeostasis was significantly compromised in pTBI compared to the Sham group. In parallel, mitochondrial membrane integrity markers, including cytochrome c (Cyt C) and voltage-dependent anion channel (VDAC), showed significant reduction over time post-pTBI. Apoptosis-responsive markers, such as glyceraldehyde 3-phosphate dehydrogenase (GAPDH) and B-cell lymphoma 2 (Bcl-2), exhibited elevated responses over time post-pTBI. Conclusions: Our results demonstrate profound insights into elevated excitotoxic mitochondrial damage after severe TBI. This time course study uncovers novel mitochondrial targets involved in TBI excitotoxicity and offers mitigation opportunities to alleviate excitotoxic responses after penetrating TBI. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Novel Therapies for Brain Injury: 2nd Edition)
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Review

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19 pages, 1540 KiB  
Review
Targeting Mitochondria in Glioma: New Hopes for a Cure
by Lidia Gatto, Vincenzo Di Nunno, Anna Ghelardini, Alicia Tosoni, Stefania Bartolini, Sofia Asioli, Stefano Ratti, Anna Luisa Di Stefano and Enrico Franceschi
Biomedicines 2024, 12(12), 2730; https://doi.org/10.3390/biomedicines12122730 - 28 Nov 2024
Cited by 2 | Viewed by 2455
Abstract
Drugs targeting mitochondrial energy metabolism are emerging as promising antitumor therapeutics. Glioma treatment is extremely challenging due to the high complexity of the tumor and the high cellular heterogeneity. From a metabolic perspective, glioma cancer cells can be classified into the oxidative metabolic [...] Read more.
Drugs targeting mitochondrial energy metabolism are emerging as promising antitumor therapeutics. Glioma treatment is extremely challenging due to the high complexity of the tumor and the high cellular heterogeneity. From a metabolic perspective, glioma cancer cells can be classified into the oxidative metabolic phenotype (mainly depending on mitochondrial respiration for energy production) and glycolytic phenotype or “Warburg effect” (mainly depending on glycolysis). Herein, we reviewed the function of novel bio-active molecules targeting oxidative phosphorylation (OXPHOS), mitochondrial membrane potential and mitochondrial dynamics. These molecules exhibit intriguing preclinical and clinical results and have been proven to be promising candidates to be further developed for glioma therapy. However, despite these initial encouraging results, it is imperative to rigorously assess the side effects of these metabolic drugs, which have a non-negligible toxicity profile. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Novel Therapies for Brain Injury: 2nd Edition)
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