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Brain Injury: New Insights into Mechanisms and Future Promising Treatments—Second...
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Brain Injury: New Insights into Mechanisms and Future Promising Treatments—Second 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 1304

Special Issue Editors

Dr. Kristina Pilipović

E-Mail Website
Guest Editor
Faculty of Medicine, University of Rijeka, Rijeka, Croatia
Interests: traumatic brain injury; stroke; neurodegeneration; neuroinflammation; glia; nanotechnology; vesicles
Special Issues, Collections and Topics in MDPI journals
Dr. Petra Dolenec

E-Mail Website
Guest Editor
Faculty of Medicine, University of Rijeka, Rijeka, Croatia
Interests: traumatic brain injury; microglia; neurodegeneration; neuroinflammation; pharmacology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

As the area of brain injury research continues to evolve rapidly, significant strides have been made in recent years toward understanding the complex pathophysiology of acquired brain injuries. Every year, upwards of 85 million people suffer from brain injuries, primarily caused by trauma or stroke. Nevertheless, the central nervous system remains uniquely challenging to treat due to its complex structure and limited regenerative capacity. Thus far, therapeutic approaches have concentrated on minimizing injury sequelae and maximizing the function of remaining brain tissue, but they have not fully addressed the regeneration and replacement of damaged tissue.

Building upon the foundation of our previous issue, this second-edition Special Issue will focus on recent advancements and emerging strategies, including nanotechnology, tissue engineering, and other innovative approaches, to repair, regenerate, and restore central nervous system functionality. We aim to showcase cutting-edge research from preclinical and clinical studies, as well as comprehensive reviews that contextualize recent breakthroughs.

We invite submissions that investigate novel regenerative and restoration techniques, with an emphasis on bridging neuronal gaps, reconnecting severed neural pathways, and promoting neural tissue regeneration. Additionally, we encourage studies that uncover new insights into the neuropathological molecular mechanisms underlying brain injury, providing a foundation for future targeted therapies.

Through this Special Issue, we hope to provide insight into the research efforts that move us closer to fully functional regenerative solutions for brain injuries. We look forward to your contributions as we collectively advance the science of brain injury treatment and neuroregeneration.

Dr. Kristina Pilipović
Dr. Petra Dolenec
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. 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

  • acquired brain injury
  • nanomedicine
  • nanotechnology
  • neuroregenerative therapy
  • neurorepair
  • new and emerging treatments
  • pharmacotherapy
  • stroke
  • tissue engineering
  • traumatic brain injury

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Related Special Issue

Published Papers (2 papers)

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Research

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17 pages, 7530 KiB  
Article
Mechanisms Underlying Hyperexcitability: Combining Mossy Fiber Sprouting and Mossy Cell Loss in Neural Network Model of the Dentate Gyrus
by Dariusz Świetlik
Biomedicines 2025, 13(6), 1416; https://doi.org/10.3390/biomedicines13061416 - 9 Jun 2025
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Abstract
Background/Objectives: A concussive head injury increases the likelihood of temporal lobe epilepsy through mechanisms that are not entirely understood. This study aimed to investigate how two key histopathological features shared by both TLE (temporal lobe epilepsy) and head injury—mossy fiber sprouting and [...] Read more.
Background/Objectives: A concussive head injury increases the likelihood of temporal lobe epilepsy through mechanisms that are not entirely understood. This study aimed to investigate how two key histopathological features shared by both TLE (temporal lobe epilepsy) and head injury—mossy fiber sprouting and hilar excitatory cell loss—contribute to the modulation of dentate gyrus excitability. Methods: A computational approach was used to explore the impact of specific levels of mossy fiber sprouting and mossy cell loss, while avoiding the confounding effects of concurrent changes. The dentate gyrus model consists of 500 granule cells, 15 mossy cells, 6 basket cells and 6 hilar perforant path-associated cells. Results: My simulations demonstrate a correlation between the degree of mossy fiber sprouting and the number of spikes in dentate gyrus granule cells (correlations coefficient R = 0.95, p < 0.0001) and other cells (correlations coefficient R = 0.99, p < 0.0001). The mean values (standard deviation, SD) and 95% CI for granule cell activity in the control group and percentage 10–50% of mossy fiber sprouting groups are 376.4 (16.7) (95% CI, 374.9–377.8) vs. 463.5 (24.3) (95% CI, 461.4–465.6) vs. 514.8 (32.5) (95% CI, 511.9–517.6) vs. 555.0 (40.4) (95% CI, 551.5–558.6) vs. 633.4 (51.8) (95% CI, 628.8–637.9) vs. 701.7 (66.2) (95% CI, 695.9–707.5). The increase in mossy fiber sprouting was significantly statistically associated with an increase in granule cell activity (p < 0.01). The removal of mossy cells led to a reduction in excitability within the model network (for granule cells, correlations coefficient R = −0.40, p < 0.0001). Conclusions: These results are generally consistent with experimental observations, which indicate a high degree of mossy fiber sprouting in animals with a higher frequency of seizures. Whereas unlike the strong hyperexcitability effects induced by mossy fiber sprouting, the removal of mossy cells led to reduced granule cell responses to perforant path activation. Full article
(This article belongs to the Special Issue Brain Injury: New Insights into Mechanisms and Future Promising Treatments—Second Edition)
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Review

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44 pages, 891 KiB  
Review
Aquaporins in Acute Brain Injury: Insights from Clinical and Experimental Studies
by Stelios Kokkoris, Charikleia S. Vrettou, Nikolaos S. Lotsios, Vasileios Issaris, Chrysi Keskinidou, Kostas A. Papavassiliou, Athanasios G. Papavassiliou, Anastasia Kotanidou, Ioanna Dimopoulou and Alice G. Vassiliou
Biomedicines 2025, 13(6), 1406; https://doi.org/10.3390/biomedicines13061406 - 7 Jun 2025
Viewed by 708
Abstract
Aquaporins (AQPs) are a family of transmembrane water channel proteins facilitating the transport of water and, in some cases, small solutes such as glycerol, lactate, and urea. In the central nervous system (CNS), several aquaporins play crucial roles in maintaining water homeostasis, modulating [...] Read more.
Aquaporins (AQPs) are a family of transmembrane water channel proteins facilitating the transport of water and, in some cases, small solutes such as glycerol, lactate, and urea. In the central nervous system (CNS), several aquaporins play crucial roles in maintaining water homeostasis, modulating cerebrospinal fluid (CSF) circulation, regulating energy metabolism, and facilitating neuroprotection under pathological conditions. Among them, AQP2, AQP4, AQP9, and AQP11 have been implicated in traumatic and non-traumatic brain injuries. The most abundant aquaporin (AQP) in the brain, AQP4, is essential for fluid regulation, facilitating water transport across the blood–brain barrier and glymphatic clearance. AQP2 is primarily known for its function in the kidneys, but it is also expressed in brain regions related to vasopressin signaling and CSF dynamics. AQP9 acts as a channel for glycerol and lactate, thus playing a role in metabolic adaptation during brain injury. AQP11, an intracellular aquaporin, is involved in oxidative stress responses and cellular homeostasis, with emerging evidence suggesting its role in neuroprotection. Aquaporins play a dual role in brain injury; while they help maintain homeostasis, their dysregulation can exacerbate cerebral edema, metabolic dysfunction, and inflammation. In traumatic brain injury (TBI), aquaporins regulate the formation and resolution of cerebral edema. In non-traumatic brain injuries, including ischemic stroke, aneurysmal subarachnoid hemorrhage (aSAH), and intracerebral hemorrhage (ICH), aquaporins influence fluid balance, energy metabolism, and oxidative stress responses. Understanding the specific roles of AQP2, AQP4, AQP9, and AQP11 in these brain injuries may lead to new therapeutic strategies to mitigate secondary damage and improve neurological outcomes. This review explores the function of the above aquaporins in both traumatic and non-traumatic brain injuries, highlighting their potential and limitations as therapeutic targets for neuroprotection and recovery. Full article
(This article belongs to the Special Issue Brain Injury: New Insights into Mechanisms and Future Promising Treatments—Second Edition)
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