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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 "Cellular Neuroscience".

Deadline for manuscript submissions: 31 December 2025 | Viewed by 9436

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 250 words) can be sent to the Editorial Office for assessment.

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 (6 papers)

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Research

Jump to: Review

20 pages, 2438 KB  
Article
EPO-R76E Enhances Retinal Pigment Epithelium Viability Under Mitochondrial Oxidative Stress Induced by Paraquat
by Jemima Alam, Alekhya Ponnam, Arusmita Souvangini, Sundaramoorthy Gopi, Cristhian J. Ildefonso and Manas R. Biswal
Cells 2025, 14(22), 1794; https://doi.org/10.3390/cells14221794 - 14 Nov 2025
Viewed by 405
Abstract
Age-related macular degeneration (AMD) is a leading cause of irreversible vision loss, primarily driven by oxidative stress–induced degeneration of retinal pigment epithelium (RPE). Erythropoietin (EPO), a hematopoietic cytokine with neuroprotective properties, has been shown to reduce apoptosis and retinal degeneration. In this study, [...] Read more.
Age-related macular degeneration (AMD) is a leading cause of irreversible vision loss, primarily driven by oxidative stress–induced degeneration of retinal pigment epithelium (RPE). Erythropoietin (EPO), a hematopoietic cytokine with neuroprotective properties, has been shown to reduce apoptosis and retinal degeneration. In this study, we examined the cytoprotective role of a non-erythropoietic EPO variant, EPO-R76E, in suppressing oxidative stress and mitochondrial dysfunction related to oxidative stress in RPE cells. Stable ARPE-19 cell lines expressing EPO-R76E were generated via lentiviral transduction and exposed to paraquat to induce oxidative stress. Oxidative stress was induced using paraquat. EPO-R76E expression conferred increased cell viability and resistance to mitochondrial damage, as assessed by cytotoxicity assays. Western blot analysis revealed reduced expression of ferritin and p62/SQSTM1, diminished activation of p-AMPK and NRF2, and restoration of GPX4 levels, indicating enhanced antioxidant defenses. Moreover, intracellular iron accumulation and reactive oxygen species were significantly reduced in EPO-R76E-expressing cells exposed to paraquat. These findings suggest that EPO-R76E promotes mitochondrial homeostasis and modulates oxidative stress pathways. Our study positions EPO-R76E as a promising therapeutic candidate for halting RPE degeneration in AMD. 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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19 pages, 4019 KB  
Article
Three-Dimensional PET Imaging Reveals Canal-like Networks for Amyloid Beta Clearance to the Peripheral Lymphatic System
by Giselle Shim, Rudolf Hall, Zeming Zhang, Ibrahim M. Shokry, Alexandra To, Lillian Cruz, Mary C. Adam, Howard Prentice, Jang-Yen Wu, Hongbo Su, Rui Tao and for the Alzheimer’s Disease Neuroimaging Initiative
Cells 2025, 14(22), 1754; https://doi.org/10.3390/cells14221754 - 10 Nov 2025
Viewed by 802
Abstract
18F-Florbetapir PET imaging is widely used to assess amyloid-β (Aβ) burden in the brain, particularly in the context of Alzheimer’s disease (AD). Conventional assessments typically rely on selected individual slices, which may limit spatial accuracy and are prone to image blurring. In [...] Read more.
18F-Florbetapir PET imaging is widely used to assess amyloid-β (Aβ) burden in the brain, particularly in the context of Alzheimer’s disease (AD). Conventional assessments typically rely on selected individual slices, which may limit spatial accuracy and are prone to image blurring. In the present study, we introduce novel techniques to enhance the spatial resolution and clarity of Aβ signal visualization in individuals pretreated with 18F-florbetapir. PET scans were retrospectively obtained from the Imaging and Data Archive for twelve individuals, including six cognitively unimpaired subjects and six diagnosed with AD. Each dataset consisted of 346 raw images, comprising 90 axial, 128 coronal, and 128 sagittal slices. Images were reconstructed into a single 3D volume using the 3D Slicer platform. Crucially, we applied artificial intelligence or AI-driven signal enhancement techniques to suppress background noise and amplify Aβ signals. This AI-enhanced processing improved image clarity and enabled visualization of subtle and spatially organized signal patterns. To verify anatomical location, Aβ PET signals were registered with MRI. This integrated workflow allowed us to visualize Aβ signals across regions of interest, including the brain parenchyma, skull, and cervical tissues. Our analytical approaches revealed that Aβ signals are highly concentrated and confined within non-CNS fluid compartments, forming canal-like networks that extend from the brain parenchyma toward the skull base, particularly the occipital clivus, and connect to the cervical lymph nodes. Additional Aβ signals were observed along the internal carotid plexus. These findings suggest that, when reconstruction in 3D and enhanced with AI, 18F-florbetapir PET imaging may not only reflect Aβ plaque burden in the brain but also visualize soluble Aβ species concentrated within anatomical clearance pathways leading to the peripheral lymphatic system. This approach offers a new dimension to PET signal interpretation and highlights the potential of AI-enhanced 3D in advancing neuroimaging analysis. 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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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 1810
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 10 | Viewed by 4088
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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20 pages, 695 KB  
Review
Retinal Neurovascular Coupling: From Mechanisms to a Diagnostic Window into Brain Disorders
by Wen Shen
Cells 2025, 14(22), 1798; https://doi.org/10.3390/cells14221798 - 16 Nov 2025
Viewed by 774
Abstract
Retinal neurovascular coupling reflects the precise coordination between neuronal activity, glial support, and vascular responses, mirroring key neurovascular mechanisms in the brain. This review emphasizes the cellular and molecular processes underlying retinal neurovascular coupling and positions the retina as a sensitive and accessible [...] Read more.
Retinal neurovascular coupling reflects the precise coordination between neuronal activity, glial support, and vascular responses, mirroring key neurovascular mechanisms in the brain. This review emphasizes the cellular and molecular processes underlying retinal neurovascular coupling and positions the retina as a sensitive and accessible model for investigating neurovascular function in the brain. It highlights how parallel neurovascular degeneration in the brain and retina provides critical insights into the pathophysiology of neurodegenerative and vascular disorders. Advances in retinal imaging, including functional optical coherence tomography (fOCT), OCT angiography (OCTA), and functional electrophysiology, offer unprecedented opportunities to detect early neuronal and vascular dysfunction, establishing the retina as a non-invasive biomarker for early detection, disease monitoring, and therapeutic evaluation in Alzheimer’s, Parkinson’s and Huntington’s disease, and stroke. By integrating structural, functional, and mechanistic approaches, the review emphasizes the retina’s potential as a translational platform bridging basic science and clinical applications in neurovascular research. 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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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 1063
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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