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Biomolecules
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Advancing Molecular Regulation in Brain Injury Research: Mechanisms, Diagnosis, and...
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Advancing Molecular Regulation in Brain Injury Research: Mechanisms, Diagnosis, and Rehabilitation

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

Deadline for manuscript submissions: 28 February 2026 | Viewed by 2988

Special Issue Editors

Dr. Guanglin Zhang

E-Mail Website
Guest Editor
Department of Integrative Biology and Physiology, University of California, Los Angeles, CA, USA
Interests: metabolic syndrome; microbiome; next-generation sequencing; neurodegenerative diseases
Special Issues, Collections and Topics in MDPI journals
Dr. Pavan Thapak

E-Mail Website
Guest Editor
Department of Neurosurgery and Integrative Biology and Physiology, UCLA BIRC, University of California, Los Angeles, CA, USA
Interests: to understand the cellular and molecular dynamics underlying neurodegenerative disorders associated with drug discovery

Special Issue Information

Dear Colleagues,

Brain injury is associated with long-term neurological infirmities and remains an unsolved health calamity affecting domestic, military, and sporting environments worldwide. Brain injury involves a multifaceted cascade of events triggered by primary and secondary pathogenesis. These events include metabolic depression, excitotoxicity, inflammation, oxidative stress, BBB leakage and others. In recent years, it has been discovered that brain injury also affects the peripheral organs’ physiology such as the liver, intestine and intestinal microbiota which further impede the recovery of injury. Despite the tremendous progress in research and evidence-based therapies, brain injury remains the leading cause of morbidity and mortality worldwide. Therefore, understanding molecular regulation among the different brain regions and the interactions between the CNS and peripheral organs is instrumental for the treatment of brain injury.

This Special Issue aims to explore the latest research findings in the pathophysiology of brain injury, biomarkers of diagnosis and prognosis, novel drug targets and translational approaches, as well as state-of-the-art reviews to drive advancements in molecular regulation of brain injury pathogenesis to facilitate the early diagnosis and clinical management of brain injury.

Research areas may include (but are not limited to) the following:

  1. Understand the cellular and molecular pathological responses instrumental to brain injury.
  2. Identify novel biomarkers and imaging techniques for diagnosis and prognosis to brain injury.
  3. Discover therapeutic targets for the prevention and treatment of brain injury.
  4. Develop strategies of rehabilitation for the recovery of patients.

Dr. Guanglin Zhang
Dr. Pavan Thapak
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. 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

  • brain injury
  • biomarkers
  • neurodegeneration
  • neuroplasticity
  • neuroimaging
  • microbial dysbiosis
  • gut–brain axis
  • cognitive rehabilitation

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Published Papers (3 papers)

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Research

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15 pages, 6783 KB  
Article
Upregulation of GLT-1 Expression Attenuates Neuronal Apoptosis and Cognitive Dysfunction via Inhibiting the CB1-CREB Signaling Pathway in Mice with Traumatic Brain Injury
by Bin Bu, Ruiyao Ma, Chengyu Wang, Shukun Jiang and Xiaoming Xu
Biomolecules 2025, 15(10), 1408; https://doi.org/10.3390/biom15101408 - 2 Oct 2025
Viewed by 261
Abstract
Background: Glutamate transporter 1 (GLT-1) plays a vital role in maintaining glutamate homeostasis in the body. A decreased GLT-1 expression in astrocytes can heighten neuronal sensitivity to glutamate excitotoxicity after traumatic brain injury (TBI). Despite its significance, the mechanisms behind the reduced expression [...] Read more.
Background: Glutamate transporter 1 (GLT-1) plays a vital role in maintaining glutamate homeostasis in the body. A decreased GLT-1 expression in astrocytes can heighten neuronal sensitivity to glutamate excitotoxicity after traumatic brain injury (TBI). Despite its significance, the mechanisms behind the reduced expression of GLT-1 following TBI remain poorly understood. After TBI, the endocannabinoid 2-arachidonoyl glycerol (2-AG) is elevated several times. 2-AG is known to inhibit key positive transcriptional regulators of GLT-1. This study aims to investigate the role of 2-AG in regulating GLT-1 expression and to uncover the underlying mechanisms involved. Methods: A controlled cortical impact (CCI) model was used to establish a TBI model in C57BL/6J mice. The CB1 receptor antagonist (referred to as AM281) and the monoacylglycerol lipase (MAGL) inhibitor (referred to as JZL184) were administered to investigate the role and mechanism of 2-AG in regulating GLT-1 expression following TBI. Behavioral tests were conducted to assess neurological functions, including the open field, Y-maze, and novel object recognition tests. Apoptotic cells were identified using the TUNEL assay, while Western blot analysis and immunofluorescence were employed to determine protein expression levels. Results: The expression of GLT-1 in the contused cortex and hippocampus following TBI showed an initial decrease, followed by a gradual recovery. It began to decrease within half an hour, reached its lowest level at 2 h, and then gradually increased, returning to normal levels by 7 days. The administration of AM281 alleviated neuronal death, improved cognitive function, and reversed the reduction of GLT-1 caused by TBI in vivo. Furthermore, 2-AG decreased GLT-1 expression in astrocytes through the CB1-CREB signaling pathway. Mechanistically, 2-AG activated CB1, which inhibited CREB phosphorylation in astrocytes. This decreased GLT-1 levels and ultimately increased neuronal sensitivity to glutamate excitotoxicity. Conclusions: Our research demonstrated that the upregulation of GLT-1 expression effectively mitigated neuronal apoptosis and cognitive dysfunction by inhibiting the CB1-CREB signaling pathway. This finding may offer a promising therapeutic strategy for TBI. Full article
(This article belongs to the Special Issue Advancing Molecular Regulation in Brain Injury Research: Mechanisms, Diagnosis, and Rehabilitation)
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35 pages, 45078 KB  
Article
Progressive Alcohol-Related Brain Atrophy and White Matter Pathology Are Linked to Long-Term Inhibitory Effects on mTOR Signaling
by Ming Tong, Camilla Homans, William Pelit, Busra Delikkaya and Suzanne M. de la Monte
Biomolecules 2025, 15(3), 413; https://doi.org/10.3390/biom15030413 - 14 Mar 2025
Cited by 2 | Viewed by 1863
Abstract
Background: Alcohol-related brain damage (ARBD) causes cognitive-behavioral impairments that can lead to dementia. White matter is a major target in ARBD. Additional research is needed to better understand the mechanisms of ARBD progression to advanced stages with permanent disability. Potential contributing factors include [...] Read more.
Background: Alcohol-related brain damage (ARBD) causes cognitive-behavioral impairments that can lead to dementia. White matter is a major target in ARBD. Additional research is needed to better understand the mechanisms of ARBD progression to advanced stages with permanent disability. Potential contributing factors include neuroinflammation and altered signaling through pathways that regulate cell survival, neuronal plasticity, myelin maintenance, and energy metabolism. Objectives: This study characterizes the time course-related effects of chronic heavy ethanol feeding on white matter myelin protein expression, neuroinflammation, and molecules that mediate signaling through the mechanistic target of rapamycin (mTOR) pathways. Methods: Adult Long Evans rats (8–12/group) were fed with isocaloric liquid diets containing 0% (control) or 36% ethanol. Experimental endpoints spanned from 1 day to 8 weeks. The frontal lobes were used for histopathology and molecular and biochemical analyses. Results: Chronic ethanol feeding caused significant brain atrophy that was detected within 4 weeks and sustained over the course of the study. Early exposure time points, i.e., 2 weeks or less, were associated with global increases in the expression of non-myelinating, myelinating, and astrocyte markers, whereas at 6 or 8 weeks, white matter oligodendrocyte/myelin/glial protein expression was reduced. These effects were not associated with shifts in neuroinflammatory markers. Instead, the early stages of ARBD were accompanied by increases in several mTOR proteins and phosphoproteins, while later phases were marked by inhibition of downstream mTOR signaling through P70S6K. Conclusions: Short-term versus long-term ethanol exposures differentially altered white matter glial protein expression and signaling through mTOR’s downstream mediators that have known roles in myelin maintenance. These findings suggest that strategic targeting of mTOR signaling dysregulation may be critical for maintaining the functional integrity of white matter and ultimately preventing long-term ARBD-related cognitive impairment. Full article
(This article belongs to the Special Issue Advancing Molecular Regulation in Brain Injury Research: Mechanisms, Diagnosis, and Rehabilitation)
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Review

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25 pages, 1871 KB  
Review
Microbiota-Derived Extracellular Vesicles as Potential Mediators of Gut–Brain Communication in Traumatic Brain Injury: Mechanisms, Biomarkers, and Therapeutic Implications
by Tarek Benameur, Abeir Hasan, Hind Toufig, Maria Antonietta Panaro, Francesca Martina Filannino and Chiara Porro
Biomolecules 2025, 15(10), 1398; https://doi.org/10.3390/biom15101398 - 30 Sep 2025
Viewed by 384
Abstract
Traumatic brain injury (TBI) remains a major global health problem, contributing significantly to morbidity and mortality worldwide. Despite advances in understanding its complex pathophysiology, current therapeutic strategies are insufficient in addressing the long-term cognitive, emotional, and neurological impairments. While the primary mechanical injury [...] Read more.
Traumatic brain injury (TBI) remains a major global health problem, contributing significantly to morbidity and mortality worldwide. Despite advances in understanding its complex pathophysiology, current therapeutic strategies are insufficient in addressing the long-term cognitive, emotional, and neurological impairments. While the primary mechanical injury is immediate and unavoidable, the secondary phase involves a cascade of biological processes leading to neuroinflammation, blood–brain barrier (BBB) disruption, and systemic immune activation. The heterogeneity of patient responses underscores the urgent need for reliable biomarkers and targeted interventions. Emerging evidence highlights the gut–brain axis as a critical modulator of the secondary phase, with microbiota-derived extracellular vesicles (MEVs) representing a promising avenue for both diagnosis and therapy. MEVs can cross the intestinal barrier and BBB, carrying biomolecules that influence neuronal survival, synaptic plasticity, and inflammatory signaling. These properties make MEVs promising biomarkers for early detection, severity classification, and prognosis in TBI, while also offering therapeutic potential through modulation of neuroinflammation and promotion of neural repair. MEV-based strategies could enable tailored interventions based on the individual’s microbiome profile, immune status, and injury characteristics. The integration of multi-omics with artificial intelligence is expected to fully unlock the diagnostic and therapeutic potential of MEVs. These approaches can identify molecular subtypes, predict outcomes, and facilitate real-time clinical decision-making. By bridging microbiology, neuroscience, and precision medicine, MEVs hold transformative potential to advance TBI diagnosis, monitoring, and treatment. This review also identifies key research gaps and proposes future directions for MEVs in precision diagnostics and gut microbiota-based therapeutics in neurotrauma care. Full article
(This article belongs to the Special Issue Advancing Molecular Regulation in Brain Injury Research: Mechanisms, Diagnosis, and Rehabilitation)
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