Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
10.6
6.0
Journals
Antioxidants
Special Issues
Revisiting the Contribution of the Nrf2 Pathway to Brain Function:...
share announcement

Revisiting the Contribution of the Nrf2 Pathway to Brain Function: Functional and Neuroprotective Actions

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: closed (30 August 2022) | Viewed by 8277

Special Issue Editor

Dr. Rodrigo A. Quintanilla

E-Mail Website
Guest Editor
Laboratory of Neurodegenerative Diseases, Instituto de Ciencias Biomedicas, Facultad de Ciencias de la Salud, Universidad Autonoma de Chile, Santiago, Chile
Interests: mitochondria; neurodegeneration; tau; Alzheimer’s disease; redox; oxidative stress

Special Issue Information

Dear Colleagues,

Brain function requires a perfect oxidation/reduction equilibrium to maintain its physiologic tasks. Mitochondria provide energy to the brain, producing large amounts of reactive oxygen species (ROS) as a secondary product. These species can directly harm neuronal cells, inducing oxidative damage observed during aging and neurodegenerative diseases. Therefore, neuronal cells present several antioxidant strategies to prevent oxidative damage, including scavenger molecules, enzymatic reactions, and molecular pathways. In this context, the Nrf2 antioxidant pathway has been considered an essential factor in reducing neuronal cells damage induced by oxidative stress and mitochondrial impairment. Interestingly, additional effects of Nrf2 have been reported, including an increase in the autophagy process, anti-inflammatory actions, and an increase in neuronal plasticity. Therefore, in this Special Issue, we will be discussing the neuroprotective actions of Nrf2 on aging and neurodegenerative diseases and the physiological functions where Nrf2 contributes to brain function.

Dr. Rodrigo A. Quintanilla
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. Antioxidants is an international peer-reviewed open access monthly 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 2900 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

  • Nrf2
  • antioxidants
  • mitochondria
  • neurodegeneration
  • synaptic loss

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • e-Book format: Special Issues with more than 10 articles can be published as dedicated e-books, ensuring wide and rapid dissemination.

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

Published Papers (2 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

Jump to: Review

16 pages, 12665 KiB  
Article
Activation of the Nrf2 Pathway Prevents Mitochondrial Dysfunction Induced by Caspase-3 Cleaved Tau: Implications for Alzheimer’s Disease
by Francisca Villavicencio-Tejo, Margrethe A. Olesen, Alejandra Aránguiz and Rodrigo A. Quintanilla
Antioxidants 2022, 11(3), 515; https://doi.org/10.3390/antiox11030515 - 8 Mar 2022
Cited by 26 | Viewed by 3984
Abstract
Alzheimer’s disease (AD) is characterized by memory and cognitive impairment, accompanied by the accumulation of extracellular deposits of amyloid β-peptide (Aβ) and the presence of neurofibrillary tangles (NFTs) composed of pathological forms of tau protein. Mitochondrial dysfunction and oxidative stress are also critical [...] Read more.
Alzheimer’s disease (AD) is characterized by memory and cognitive impairment, accompanied by the accumulation of extracellular deposits of amyloid β-peptide (Aβ) and the presence of neurofibrillary tangles (NFTs) composed of pathological forms of tau protein. Mitochondrial dysfunction and oxidative stress are also critical elements for AD development. We previously showed that the presence of caspase-3 cleaved tau, a relevant pathological form of tau in AD, induced mitochondrial dysfunction and oxidative damage in different neuronal models. Recent studies demonstrated that the nuclear factor (erythroid-derived 2)-like 2 (Nrf2) plays a significant role in the antioxidant response promoting neuroprotection. Here, we studied the effects of Nrf2 activation using sulforaphane (SFN) against mitochondrial injury induced by caspase-3 cleaved tau. We used immortalized cortical neurons to evaluate mitochondrial bioenergetics and ROS levels in control and SFN-treated cells. Expression of caspase-3 cleaved tau induced mitochondrial fragmentation, depolarization, ATP loss, and increased ROS levels. Treatment with SFN for 24 h significantly prevented these mitochondrial abnormalities, and reduced ROS levels. Analysis of Western blots and rt-PCR studies showed that SFN treatment increased the expression of several Nrf2-related antioxidants genes in caspase-3 cleaved tau cells. These results indicate a potential role of the Nrf2 pathway in preventing mitochondrial dysfunction induced by pathological forms of tau in AD. Full article
(This article belongs to the Special Issue Revisiting the Contribution of the Nrf2 Pathway to Brain Function: Functional and Neuroprotective Actions)
►▼ Show Figures

Figure 1

Review

Jump to: Research

15 pages, 1496 KiB  
Review
Neurodegeneration in Multiple Sclerosis: The Role of Nrf2-Dependent Pathways
by Paloma P. Maldonado, Coram Guevara, Margrethe A. Olesen, Juan Andres Orellana, Rodrigo A. Quintanilla and Fernando C. Ortiz
Antioxidants 2022, 11(6), 1146; https://doi.org/10.3390/antiox11061146 - 10 Jun 2022
Cited by 26 | Viewed by 3705
Abstract
Multiple sclerosis (MS) encompasses a chronic, irreversible, and predominantly immune-mediated disease of the central nervous system that leads to axonal degeneration, neuronal death, and several neurological symptoms. Although various immune therapies have reduced relapse rates and the severity of symptoms in relapsing-remitting MS, [...] Read more.
Multiple sclerosis (MS) encompasses a chronic, irreversible, and predominantly immune-mediated disease of the central nervous system that leads to axonal degeneration, neuronal death, and several neurological symptoms. Although various immune therapies have reduced relapse rates and the severity of symptoms in relapsing-remitting MS, there is still no cure for this devastating disease. In this brief review, we discuss the role of mitochondria dysfunction in the progression of MS, focused on the possible role of Nrf2 signaling in orchestrating the impairment of critical cellular and molecular aspects such as reactive oxygen species (ROS) management, under neuroinflammation and neurodegeneration in MS. In this scenario, we propose a new potential downstream signaling of Nrf2 pathway, namely the opening of hemichannels and pannexons. These large-pore channels are known to modulate glial/neuronal function and ROS production as they are permeable to extracellular Ca2+ and release potentially harmful transmitters to the synaptic cleft. In this way, the Nrf2 dysfunction impairs not only the bioenergetics and metabolic properties of glial cells but also the proper antioxidant defense and energy supply that they provide to neurons. Full article
(This article belongs to the Special Issue Revisiting the Contribution of the Nrf2 Pathway to Brain Function: Functional and Neuroprotective Actions)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-2
Back to TopTop