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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: 25 May 2024 | Viewed by 4837

Special Issue Editor


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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

Published Papers (2 papers)

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Research

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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
Viewed by 912
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 - 02 Feb 2023
Cited by 15 | Viewed by 3472
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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