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Cell Stress and Intervention in Neurological Disease: In Honor of...
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Cell Stress and Intervention in Neurological Disease: In Honor of Dr. Jang-Yen Wu for His Long and Distinguished Career in Neuroscience

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

Deadline for manuscript submissions: 31 December 2025 | Viewed by 5461

Special Issue Editors

Prof. Dr. Howard Prentice

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; neuroprotection; neurogenesis
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Jang-Yen Wu

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,

Preface: Most of the papers in this Special Issue are closely related to the International Symposium held on December 16th, 2024, at Florida Atlantic University, Boca Raton, Florida, USA. This symposium was entitled “International Symposium on Brain Function/Dysfunction and Intervention” and was held in honor of the outstanding contributions to neuroscience of Dr. Jang-Yen Wu over his long and distinguished career.

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

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. Cells is an international peer-reviewed open access semimonthly 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

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

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Published Papers (3 papers)

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Research

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17 pages, 2289 KB  
Article
Ashwagandha Root Extract Mitigates Fibromyalgia-like Symptoms via Neurochemical and Histological Modulation in Mice
by Razan Fawaz Hasanyn, Ashwaq H. Batawi, Mona A. AL-Thepyani, Reham Tash, Asma Almuhammadi, Ashwaq Hassan Alsabban and Badrah S. Alghamdi
Cells 2025, 14(18), 1478; https://doi.org/10.3390/cells14181478 - 22 Sep 2025
Viewed by 922
Abstract
Fibromyalgia syndrome (FMS) is a chronic disorder marked by widespread musculoskeletal pain, fatigue, mood disturbances, and cognitive impairments. Current treatments primarily focus on symptom management. Ashwagandha (Withania somnifera), a traditional Ayurvedic herb, is known for its adaptogenic and neuroprotective properties. This [...] Read more.
Fibromyalgia syndrome (FMS) is a chronic disorder marked by widespread musculoskeletal pain, fatigue, mood disturbances, and cognitive impairments. Current treatments primarily focus on symptom management. Ashwagandha (Withania somnifera), a traditional Ayurvedic herb, is known for its adaptogenic and neuroprotective properties. This study evaluated the protective effects of the methanolic root extract of Ashwagandha (ARE) in a reserpine-induced fibromyalgia model in male Swiss albino mice. Mice received oral ARE (100 mg/kg) for 17 days and reserpine (0.5 mg/kg, subcutaneously) for three consecutive days to induce fibromyalgia-like symptoms. Behavioral assessments included Von Frey, tail suspension, rotarod, and Y-maze tests. Histological analysis was conducted on the hippocampus and thalamus; however, neurochemical analysis focused on markers such as serotonin, norepinephrine, IL-1β, TNFα, MDA, and NO. Results indicated that ARE significantly reduced pain and depressive-like behavior and improved motor function (p < 0.0001); however, no significant changes were observed in open-field locomotion. Histological examination revealed protection of Ashwagandha against neurodegeneration and improved hippocampal integrity, accompanied by increased serotonin and norepinephrine levels and decreased pro-inflammatory cytokines. These findings suggest that Ashwagandha root extract may offer therapeutic benefits for managing fibromyalgia symptoms. Full article
(This article belongs to the Special Issue Cell Stress and Intervention in Neurological Disease: In Honor of Dr. Jang-Yen Wu for His Long and Distinguished Career in Neuroscience)
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21 pages, 23279 KB  
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
Cited by 8 | Viewed by 3332
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: In Honor of Dr. Jang-Yen Wu for His Long and Distinguished Career in Neuroscience)
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Review

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16 pages, 694 KB  
Review
Nucleus Reuniens-Elicited Delta Oscillations Disable the Prefrontal Cortex in Schizophrenia
by Robert P. Vertes and Stephanie B. Linley
Cells 2025, 14(19), 1545; https://doi.org/10.3390/cells14191545 - 3 Oct 2025
Viewed by 766
Abstract
Schizophrenia (SZ) is a severe mental disorder associated with an array of symptoms characterized as positive, negative and cognitive dysfunctions. While SZ is a multifaceted disorder affecting several regions of the brain, altered thalamocortical systems have emerged as a leading contributor to SZ. [...] Read more.
Schizophrenia (SZ) is a severe mental disorder associated with an array of symptoms characterized as positive, negative and cognitive dysfunctions. While SZ is a multifaceted disorder affecting several regions of the brain, altered thalamocortical systems have emerged as a leading contributor to SZ. Specifically, it has been shown that: (1) the thalamus is functionally disconnected from the prefrontal cortex (PFC) in SZ; (2) neural activity and blood flow to the PFC are greatly diminished in SZ (hypofrontality); and (3) delta oscillations are abnormally present in the PFC during the waking state in SZ. We suggest that the abnormal delta oscillations drive the other PFC signs of SZ. Specifically, decreases in energy required to maintain delta, would initiate the reduced PFC perfusion of SZ (hypofrontality), and contribute to the ‘mismatched’ thalamic and PFC activity of SZ. As SZ involves glutamate (NMDAR) hypofunction and dopamine hyperfunction, both NMDAR antagonists and dopamine agonists produce marked increases in delta oscillations in nucleus reuniens (RE) of the thalamus and its target structures, including the PFC. This would suggest that RE is a primary source for the elicitation of PFC delta activity, and the presence of delta during waking (together with associated signs) would indicate that the prefrontal cortex is disabled (or non-functional) in schizophrenia. Full article
(This article belongs to the Special Issue Cell Stress and Intervention in Neurological Disease: In Honor of Dr. Jang-Yen Wu for His Long and Distinguished Career in Neuroscience)
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