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Current Insights on Neuroprotection
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Current Insights on Neuroprotection

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Neurobiology".

Deadline for manuscript submissions: closed (20 January 2025) | Viewed by 12715

Special Issue Editor

Dr. Jover-Mengual Teresa

E-Mail Website
Guest Editor
Unidad Mixta de Investigación Cerebrovascular UVEG-IIS La Fe, Departament de Fisiologia, Universitat de València, Valencia, Spain
Interests: molecular; cellular; ischemic brain damage; neuroprotection; stroke

Special Issue Information

Dear Colleagues, 

Preservation of the neuronal structure and function after a neurodegenerative insult is the hallmark of neuroprotection. It involves the maintenance of neuronal integrity by preventing or decelerating neuronal loss, as well as secondary injuries, thereby slowing the progression of neurological disease. Reduced delivery of oxygen and glucose to the brain, mitocondrial dysfunction, excitotoxicity, inflammation and elevated levels of oxidative stress are all mechanisms of neuronal injury. Limiting these mechanisms is the essence of neuroprotection.

This Special Issue on neuroprotection will present new advances in some of the most common mechanisms known to trigger neuronal injury and death.

For this Special Issue, we invite research, as well as review articles, on the role of the signaling pathways involved in mitochondrial dysfunction, inflammation, excitotoxicity and oxidative stress, as well as how these pathways could be targeted as therapeutic strategies for neurodegenerative diseases.

Dr. Jover-Mengual Teresa
Guest Editor

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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • neuronal structure
  • neuronal function
  • neuroprotection
  • secondary injuries
  • oxygen
  • glucose
  • oxidative stress
  • mitochondrial dysfunction
  • inflammation
  • excitotoxicity

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Further information on MDPI's Special Issue policies can be found here.

Published Papers (5 papers)

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Research

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17 pages, 4488 KiB  
Article
Early-Life Stress Caused by Maternal Deprivation Impacts Dendritic Morphology of Adult Male Mouse Neocortical Interneurons
by Mohammed M. Nakhal, Lidya K. Yassin, Shaikha Al Houqani, Ayishal B. Mydeen, Marwa F. Ibrahim, Safa Shehab, Mohammed Z. Allouh and Mohammad I. K. Hamad
Int. J. Mol. Sci. 2025, 26(5), 1909; https://doi.org/10.3390/ijms26051909 - 23 Feb 2025
Viewed by 556
Abstract
A substantial body of research suggests that early-life stress (ELS) is associated with neuropathology in adulthood. Maternal deprivation (MD) is a commonly utilised model in mice for the study of specific neurological diseases. The appropriate growth of dendrites is essential for the optimal [...] Read more.
A substantial body of research suggests that early-life stress (ELS) is associated with neuropathology in adulthood. Maternal deprivation (MD) is a commonly utilised model in mice for the study of specific neurological diseases. The appropriate growth of dendrites is essential for the optimal functioning of the nervous system. However, the impact of ELS on interneuron dendritic morphology remains unclear. To ascertain whether ELS induces alterations in the morphology of GABAergic inhibitory interneurons in layers II/III of the medial entorhinal cortex (mEC), the somatosensory cortex (SSC), the motor cortex (MC), and the CA1 region of the hippocampus (Hp), 9-day-old male GAD-67-EGFP transgenic mice were subjected to a 24 h MD. At postnatal day 60 (P60), the animals were sacrificed, and their brains were subjected to morphological analyses. The results indicated that MD affected the dendritic morphology of GABAergic interneurons. The mean dendritic length and mean dendritic segments of the examined cortical areas, except for the MC, were significantly decreased, whereas the number of primary dendrites was unaffected. Furthermore, the density of GAD67-EGFP-positive interneurons was decreased in the mEC and Hp, but not in the somatosensory and MC. The induction of ELS through MD in a developmental time window when significant morphological changes occur rendered the developing cells particularly susceptible to stress, resulting in a significant reduction in the number of surviving interneurons at the adult stage. Full article
(This article belongs to the Special Issue Current Insights on Neuroprotection)
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14 pages, 4079 KiB  
Article
Neuroprotective Effects of Ethanol Extract Polyscias guilfoylei (EEPG) Against Glutamate Induced Neurotoxicity in HT22 Cells
by Qui Ngoc Sang Nguyen, Ki-Yeon Yoo, Thi Thu Trang Pham, Baskar Selvaraj, Huong Thuy Vu, Tam Thi Le, Heesu Lee, Quang Luc Tran, Phuong Thien Thuong, Ae Nim Pae, Sang Hoon Jung and Jae Wook Lee
Int. J. Mol. Sci. 2024, 25(22), 12153; https://doi.org/10.3390/ijms252212153 - 12 Nov 2024
Cited by 2 | Viewed by 1860
Abstract
Oxidative stress induced by glutamate is a significant contributor to neuronal cell damage and can lead to neurodegenerative diseases such as Alzheimer’s, Huntington’s, and ischemic brain injury. At the cellular level, oxidative stress increases Ca2+ ion influx and reactive oxygen species (ROS), [...] Read more.
Oxidative stress induced by glutamate is a significant contributor to neuronal cell damage and can lead to neurodegenerative diseases such as Alzheimer’s, Huntington’s, and ischemic brain injury. At the cellular level, oxidative stress increases Ca2+ ion influx and reactive oxygen species (ROS), which activate the MAPK signaling pathway. Additionally, the generation of ROS causes mitochondrial dysfunction, triggering apoptosis by promoting the translocation of AIF to the nucleus from the mitochondria. The neuroprotective potential of Polyscias guilfoylei has not yet been reported. Therefore, in this study, the ethanol extract of Polyscias guilfoylei (EEPG) was examined for its protective effect against oxidative cell damage caused by glutamate in neuronal cells. EEPG treatment increased the viability of HT22 cells exposed to high concentrations of glutamate. Cellular Ca2+ ion influx and ROS generation decreased with EEPG treatment in glutamate-treated HT22 cells. EEPG treatment inhibited MAPK activation and AIF nuclear translocation. In an in vivo study, EEPG attenuated brain cell death in an ischemic brain injury rat model. This study demonstrates the potential therapeutic effects of Polyscias guilfoylei in the treatment of ischemic brain injury. Full article
(This article belongs to the Special Issue Current Insights on Neuroprotection)
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26 pages, 18474 KiB  
Article
Neuropeptide FF Promotes Neuronal Survival and Enhances Synaptic Protein Expression Following Ischemic Injury
by In-Ae Choi, Ji Hee Yun, Jongmin Lee and Dong-Hee Choi
Int. J. Mol. Sci. 2024, 25(21), 11580; https://doi.org/10.3390/ijms252111580 - 28 Oct 2024
Cited by 1 | Viewed by 1056
Abstract
This study explores the neuroprotective effects of neuropeptide FF (NPFF, FLFQPQRFamide) in the context of ischemic injury. Based on transcriptomic analysis in stroke models treated with 5-Aza-dC and task-specific training, we identified significant gene expression changes, particularly involving NPFF. To further explore NPFF’s [...] Read more.
This study explores the neuroprotective effects of neuropeptide FF (NPFF, FLFQPQRFamide) in the context of ischemic injury. Based on transcriptomic analysis in stroke models treated with 5-Aza-dC and task-specific training, we identified significant gene expression changes, particularly involving NPFF. To further explore NPFF’s role in promoting neuronal recovery, recombinant NPFF protein (rNPFF) was used in primary mixed cortical cultures subjected to oxygen-glucose deprivation and reoxygenation. Our results demonstrated that rNPFF significantly reduced lactate dehydrogenase release, indicating decreased cellular damage. It also significantly increased the expression of TUJ1 and MAP2, markers of neuronal survival and dendritic integrity. Additionally, rNPFF significantly upregulated key synaptic proteins, including GAP43, PSD95, and synaptophysin, which are essential for synaptic repair and plasticity. Post-injury rNPFF treatment led to a significant upregulation of pro-brain-derived neurotrophic factor (BDNF) and mature BDNF, which play critical roles in neuronal survival, growth, and synaptic plasticity. Moreover, rNPFF activated the protein kinase Cε isoform, Sirtuin 1, and peroxisome proliferator-activated receptor gamma pathways, which are crucial for regulating cellular stress responses, synaptic plasticity, and energy homeostasis, further promoting neuronal survival and recovery. These findings suggest that rNPFF may play a pivotal role in enhancing neuronal survival and synaptic plasticity after ischemic injury, highlighting its potential as a therapeutic target for stroke recovery. Full article
(This article belongs to the Special Issue Current Insights on Neuroprotection)
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18 pages, 2560 KiB  
Article
Cerebroprotective Effect of 17β-Estradiol Replacement Therapy in Ovariectomy-Induced Post-Menopausal Rats Subjected to Ischemic Stroke: Role of MAPK/ERK1/2 Pathway and PI3K-Independent Akt Activation
by María C. Burguete, Teresa Jover-Mengual, María Castelló-Ruiz, Mikahela A. López-Morales, José M. Centeno, Alicia Aliena-Valero, Enrique Alborch, Germán Torregrosa and Juan B. Salom
Int. J. Mol. Sci. 2023, 24(18), 14303; https://doi.org/10.3390/ijms241814303 - 19 Sep 2023
Cited by 2 | Viewed by 1754
Abstract
Despite the overwhelming advances in the understanding of the pathogenesis of stroke, a devastating disease affecting millions of people worldwide, currently there are only a limited number of effective treatments available. Preclinical and clinical studies show that stroke is a sexually dimorphic disorder, [...] Read more.
Despite the overwhelming advances in the understanding of the pathogenesis of stroke, a devastating disease affecting millions of people worldwide, currently there are only a limited number of effective treatments available. Preclinical and clinical studies show that stroke is a sexually dimorphic disorder, affecting males and females differently. Strong experimental evidence indicates that estrogen may play a role in this difference and that exogenous 17β-estradiol (E2) is neuroprotective against stroke in both male and female rodents. However, the molecular mechanisms by which E2 intervenes in ischemia-induced cell death, revealing these sex differences, remain unclear. The present study was aimed to determine, in female rats, the molecular mechanisms of two well-known pro-survival signaling pathways, MAPK/ERK1/2 and PI3K/Akt, that mediate E2 neuroprotection in response to acute ischemic stroke. E2 pretreatment reduced brain damage and attenuated apoptotic cell death in ovariectomized female rats after an ischemic insult. Moreover, E2 decreased phosphorylation of ERK1/2 and prevented ischemia/reperfusion-induced dephosphorylation of both Akt and the pro-apoptotic protein, BAD. However, MAPK/ERK1/2 inhibitor PD98059, but not the PI3K inhibitor LY294002, attenuated E2 neuroprotection. Thus, these results suggested that E2 pretreatment in ovariectomized female rats modulates MAPK/ERK1/2 and activates Akt independently of PI3K to promote cerebroprotection in ischemic stroke. A better understanding of the mechanisms and the influence of E2 in the female sex paves the way for the design of future successful hormone replacement therapies. Full article
(This article belongs to the Special Issue Current Insights on Neuroprotection)
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Review

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18 pages, 1509 KiB  
Review
Advanced Glycation End-Products and Diabetic Neuropathy of the Retina
by Toshiyuki Oshitari
Int. J. Mol. Sci. 2023, 24(3), 2927; https://doi.org/10.3390/ijms24032927 - 2 Feb 2023
Cited by 36 | Viewed by 6467
Abstract
Diabetic retinopathy is a tissue-specific neurovascular impairment of the retina in patients with both type 1 and type 2 diabetes. Several pathological factors are involved in the progressive impairment of the interdependence between cells that consist of the neurovascular units (NVUs). The advanced [...] Read more.
Diabetic retinopathy is a tissue-specific neurovascular impairment of the retina in patients with both type 1 and type 2 diabetes. Several pathological factors are involved in the progressive impairment of the interdependence between cells that consist of the neurovascular units (NVUs). The advanced glycation end-products (AGEs) are one of the major pathological factors that cause the impairments of neurovascular coupling in diabetic retinopathy. Although the exact mechanisms for the toxicities of the AGEs in diabetic retinopathy have not been definitively determined, the AGE-receptor of the AGE (RAGE) axis, production of reactive oxygen species, inflammatory reactions, and the activation of the cell death pathways are associated with the impairment of the NVUs in diabetic retinopathy. More specifically, neuronal cell death is an irreversible change that is directly associated with vision reduction in diabetic patients. Thus, neuroprotective therapies must be established for diabetic retinopathy. The AGEs are one of the therapeutic targets to examine to ameliorate the pathological changes in the NVUs in diabetic retinopathy. This review focuses on the basic and pathological findings of AGE-induced neurovascular abnormalities and the potential therapeutic approaches, including the use of anti-glycated drugs to protect the AGE-induced impairments of the NVUs in diabetic retinopathy. Full article
(This article belongs to the Special Issue Current Insights on Neuroprotection)
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