Editorial Board Collection Series: Innovative Research in Molecular and Cellular Neuroscience for Regulation of Cell Death Mechanisms for Functional Neuroprotection

A special issue of Brain Sciences (ISSN 2076-3425). This special issue belongs to the section "Molecular and Cellular Neuroscience".

Deadline for manuscript submissions: 31 March 2026 | Viewed by 555

Special Issue Editor


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Department of Pathology, Microbiology, and Immunology, University of South Carolina School of Medicine, Columbia, SC 29209, USA
Interests: apoptosis; angiogenesis; autophagy; chemotherapy; CRISPR technology; epigenetics; glioblastoma; immunotherapy; miRNAs; photodynamic therapy; RNA interference technology
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Special Issue Information

Dear Colleagues,

Neurodegeneration caused by the deregulation of different cell death mechanisms is a common feature of all diseases and injuries in the nervous system. The identification of deregulated cell death mechanisms and their regulation by pharmacological and technological means may promote neurological and cognitive functions. Recent advances in molecular and cellular neuroscience, alongside technological breakthroughs, could enable the achievement of functional neuroprotection in major neurological diseases such as Alzheimer’s disease (AD), amyotrophic lateral sclerosis (ALS), epilepsy or seizure disorder (SD), Huntington’s disease (HD), Parkinson’s disease (PD), and multiple sclerosis (MS), and injuries such as traumatic brain injury (TBI), spinal cord injury (SCI), and ischemic brain injury (IBI).

This Special Issue of Brain Sciences will consider all aspects of molecular and cellular neuroscience research concerning the regulation of cell death mechanisms for functional neuroprotection in any major neurological diseases and injuries. Investigators in the field of Molecular and Cellular Neuroscience are cordially invited to submit their innovative research and review articles to this exciting Special Issue of Brain Sciences. We sincerely hope that today’s breakthroughs in preclinical research will bring tomorrow’s treatments to the clinic in order to provide functional neuroprotection in all diseases and injuries of the nervous system.

Prof. Dr. Swapan K. Ray
Guest Editor

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Keywords

  • apoptosis
  • autophagy
  • artificial intelligence
  • CRISPR
  • demyelination
  • ferroptosis
  • inflammasomes
  • microRNAs
  • necrosis
  • neuroprotection
  • organoids
  • PANoptosis
  • animal and cellular models of neurological diseases and injuries
  • proteases

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Published Papers (1 paper)

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Research

9 pages, 588 KB  
Communication
Differential Neuroendocrine Responses and Dysregulation of the Hypothalamic–Pituitary–Adrenal Axis Following Repeated Mild Concussive Impacts and Blast Exposures in a Rat Model
by Rex Jeya Rajkumar Samdavid Thanapaul, Jishnu K. S. Krishnan, Manoj Y. Govindarajulu, Chetan Y. Pundkar, Gaurav Phuyal, Joseph B. Long and Peethambaran Arun
Brain Sci. 2025, 15(8), 847; https://doi.org/10.3390/brainsci15080847 - 8 Aug 2025
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Abstract
Traumatic brain injury (TBI) remains a significant public health concern, particularly among military personnel and contact sport athletes who are frequently exposed to repeated blast overpressure waves and mild concussive impacts, respectively. While moderate and severe TBIs have been extensively studied, the long-term [...] Read more.
Traumatic brain injury (TBI) remains a significant public health concern, particularly among military personnel and contact sport athletes who are frequently exposed to repeated blast overpressure waves and mild concussive impacts, respectively. While moderate and severe TBIs have been extensively studied, the long-term neuroendocrine consequences of mild, repetitive brain trauma are poorly understood. In this study, we investigated the temporal dynamics of hypothalamic–pituitary–adrenal (HPA) axis dysregulation following repeated mild concussive head impacts and blast exposures using two clinically relevant rodent models. Male Sprague-Dawley rats were subjected to repeated mild concussive impacts using a modified weight drop model or repeated blast exposures using an advanced blast simulator. Plasma levels of adrenocorticotropic hormone (ACTH) and corticosterone were measured on days 1 and 30 post-injuries. Our findings revealed that repeated blast exposures induced elevation of plasma ACTH and corticosterone on days 1 and 30 post-blasts. After the repeated mild concussive impacts, increased plasma levels of corticosterone were observed on days 1 and 30, but ACTH levels were increased only on day 30. This study is among the first to directly compare neuroendocrine outcomes of repeated mild concussive impacts and blast exposures within a unified experimental framework. Our findings demonstrate distinct temporal trajectories of HPA axis dysregulation depending on injury type and highlight plasma levels of ACTH and corticosterone as potential biomarkers of subclinical brain trauma. These insights may inform early diagnostic approaches and therapeutic strategies aimed at mitigating long-term stress-related complications following mild traumatic brain injuries. Full article
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