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Special Issue Editor

Dr. Rodrigo A. Quintanilla

Laboratory of Neurodegenerative Diseases, Centro de Investigación Biomédica, Universidad Autónoma de Chile. El LLano Subercaseaux 2801, San Miguel, Santiago 8910060, Chile
Interests: mitochondria; neurodegeneration; Tau; Alzheimer´s disease

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

Published Papers (2 papers)

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Research

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16 pages, 12665 KiB

Open AccessArticle

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://0-doi-org.brum.beds.ac.uk/10.3390/antiox11030515 - 08 Mar 2022

Cited by 16 | Viewed by 2848

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 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)

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Review

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15 pages, 1496 KiB

Open AccessReview

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://0-doi-org.brum.beds.ac.uk/10.3390/antiox11061146 - 10 Jun 2022

Cited by 9 | Viewed by 2419

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, 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)

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