Cell Stress and Intervention in Neurological Disease

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cells of the Nervous System".

Deadline for manuscript submissions: 20 August 2025 | Viewed by 1613

Special Issue Editors


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Guest Editor
Charles E. Schmidt College of Medicine, Florida Atlantic University, Boca Raton, FL 33431-0991, USA
Interests: stroke; Alzheimer’s disease; gene therapy; neuroprotection; neurogenesis
Special Issues, Collections and Topics in MDPI journals

E-Mail Website
Guest Editor
Charles E. Schmidt College of Medicine, Florida Atlantic University, Boca Raton, FL 33431-0991, USA
Interests: stroke; Alzheimer’s disease; gene therapy; neurotransmitters; neuroprotection; neurogenesis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Major neurological disorders, including stroke, neurodegenerative diseases, and neuropsychiatric disorders, are characterized by processes involving the over-excitation of neurons as well as the dysregulation of ion channels, vascular and immune systems, and oxidative stress. This Special Issue provides analyses of the pathological processes associated with several of these diseases, such as Alzheimer's disease, stroke, and key developmental disorders, with a focus on (1) cell stress and cell death processes including mitochondrial stress, apoptosis, autophagy, and ER stress, (2) pro-survival mechanisms such as neuroprotective pathways and stem cell mobilization and multicellular communication, and (3) potential therapeutic interventions based on the mechanism associated with these diseases such as gene therapy, enhanced growth factor action, neurotrophic regulation, immunomodulatory approaches and therapeutics to inhibit neuronal excitotoxicity and cell death programs. In addition, new delivery methods that could circumvent the blood–brain barrier are also included as part of the solution for therapeutic intervention of brain diseases. The topic of multicellular communication (neurons, astrocytes, microglia, and vascular cells) to be addressed in this issue is also critical in providing insights into therapeutic processes as well as advancing knowledge in neuronal protection and neurogenesis in general.

For this Special Issue, we welcome the submission of original articles and reviews in the neuroscience field, highlighting cell survival, neurotrophic action, cell–cell communication, neuro-regeneration processes, and immunomodulatory targeting.

Prof. Dr. Howard Prentice
Prof. Dr. Jang-Yen Wu
Guest Editors

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Keywords

  • neurodegenerative disease
  • gene therapy
  • excitotoxicity
  • calcium dysregulation
  • Alzheimer’s disease
  • stroke
  • neuroprotection
  • neurogenesis

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Published Papers (1 paper)

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Research

21 pages, 23279 KiB  
Article
Effects of Microplastic Accumulation on Neuronal Death After Global Cerebral Ischemia
by Dong Yeon Kim, Min Kyu Park, Hyun Wook Yang, Seo Young Woo, Hyun Ho Jung, Dae-Soon Son, Bo Young Choi and Sang Won Suh
Cells 2025, 14(4), 241; https://doi.org/10.3390/cells14040241 - 7 Feb 2025
Viewed by 1447
Abstract
Brain ischemia, a condition in which the brain is deprived of blood flow, can lead to a stroke due to blocked or unstable blood vessels. Global cerebral ischemia (GCI), characterized by an interruption in blood flow, deprives the brain of oxygen and nutrients, [...] Read more.
Brain ischemia, a condition in which the brain is deprived of blood flow, can lead to a stroke due to blocked or unstable blood vessels. Global cerebral ischemia (GCI), characterized by an interruption in blood flow, deprives the brain of oxygen and nutrients, producing reactive oxygen species (ROS) that trigger cell death, which kills nerve cells. Microplastics (MPs), tiny environmental pollutants, can enter the human body through contaminated food, water, disposable items, cosmetics, and more. Once in the brain, MPs can increase neuroinflammation by overstimulating inflammatory factors such as microglia. MPs can also damage neurons by scratching myelin and microtubules, slowing signal transduction, causing cognitive impairment, and leading to neuronal death. Furthermore, microtubule damage may result in the release of phosphorylated tau proteins, potentially linked to Alzheimer’s disease. We hypothesized that MPs could exacerbate neuroinflammation and microtubule destruction after GCI, leading to increased neuronal death. To test this hypothesis, we administered MPs (0.5 µm) orally at a dose of 50 mg/kg before and after inducing GCI. Staining techniques such as Fluoro-Jade B (FJB), ionized calcium-binding adaptor molecule 1 (Iba-1), cluster of differentiation 68 (CD68), myelin basic protein (MBP), and microtubule-associated protein 2 (MAP2) were used, along with Western blot analysis for interleukin-6 (IL-6), TNF-α, tau-5, and phospho-tau (S396) to evaluate the effects of MPs on neuronal cell death, neuroinflammation, and microtubule destruction. The results showed that MP accumulation significantly increased neuroinflammation, microtubule disruption, and neuronal cell death in the GCI-MP group compared to the GCI-vehicle group. Therefore, this study suggests that MP accumulation in daily life may contribute to the exacerbation of the disease, potentially leading to severe neuronal cell death after GCI. Full article
(This article belongs to the Special Issue Cell Stress and Intervention in Neurological Disease)
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