Mitochondrial Metabolism in Neural Regeneration

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 (31 December 2021) | Viewed by 9774

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Guest Editor
Research Institute for Medicines (iMed.ULisboa), Faculty of Pharmacy, Universidade de Lisboa, 1649-003 Lisbon, Portugal
Interests: aging; bioenergetics; cell signaling; mitochondrial metabolism; neural stem cell fate; neuroregeneration
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Special Issue Information

Dear Colleagues,

The brain is one of the most metabolically active organs in the human body. In fact, the vast majority of neurological disorders are somehow related with disturbed mitochondrial energetic metabolism. In turn, stem cell therapy is a strategy that is currently far from being satisfactory and applied in the field of clinical neuroscience. The poor survival and differentiation levels of neural stem cells (NSCs) during aging or neural injury have been one of the major drawbacks. Notably, recent studies have shown that mitochondrial metabolism is pivotal in regulating NSC-mediated neural regeneration and neuroprotection, where the mitochondrial oxidative state plays a key role in these processes. Therefore, a better understanding of the mitochondrial mechanisms and therapeutic approaches responsible for the long-term survival, differentiation, and synaptic integration of newborn neurons may represent a step in the right direction. We invite investigators to contribute original studies and review articles that boost the improvement of neural replacement therapies by targeting mitochondria, oxidative state, and cellular metabolism. We are interested in articles from basic research to clinical application to foster the proliferation, differentiation, maturation, and functional integration of NSCs and/or new neural cells in both animals and human models.

Dr. Susana Solá
Guest Editor

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Keywords

  • Bioenergetics
  • Diet
  • Mitochondrial metabolism
  • Neuroregeneration
  • Neural stem cell fate

Published Papers (2 papers)

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Review

14 pages, 895 KiB  
Review
Clinical Diagnosis and Treatment of Leigh Syndrome Based on SURF1: Genotype and Phenotype
by Inn-Chi Lee and Kuo-Liang Chiang
Antioxidants 2021, 10(12), 1950; https://doi.org/10.3390/antiox10121950 - 05 Dec 2021
Cited by 5 | Viewed by 5376
Abstract
SURF1 encodes the assembly factor for maintaining the antioxidant of cytochrome c oxidase (COX) stability in the human electron respiratory chain. Mutations in SURF1 can cause Leigh syndrome (LS), a subacute neurodegenerative encephalopathy, characterized by early onset (infancy), grave prognosis, and predominant symptoms [...] Read more.
SURF1 encodes the assembly factor for maintaining the antioxidant of cytochrome c oxidase (COX) stability in the human electron respiratory chain. Mutations in SURF1 can cause Leigh syndrome (LS), a subacute neurodegenerative encephalopathy, characterized by early onset (infancy), grave prognosis, and predominant symptoms presenting in the basal ganglia, thalamus, brainstem, cerebellum, and peripheral nerves. To date, more than sixty different SURF1 mutations have been found to cause SURF1-associated LS; however, the relationship between genotype and phenotype is still unclear. Most SURF1-associated LS courses present as typical LS and cause early mortality (before the age of ten years). However, 10% of the cases present with atypical courses with milder symptoms and increased life expectancy. One reason for this inconsistency may be due to specific duplications or mutations close to the C-terminus of the SURF1 protein appearing to cause less protein decay. Furthermore, the treatment for SURF1-associated LS is unsatisfactory. A ketogenic diet is most often prescribed and has proven to be effective. Supplementing with coenzyme Q and other cofactors is also a common treatment option; however, the results are inconsistent. Importantly, anti-epileptic drugs such as valproate—which cause mitochondrial dysfunction—should be avoided in patients with SURF1-associated LS presenting with seizures. Full article
(This article belongs to the Special Issue Mitochondrial Metabolism in Neural Regeneration)
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22 pages, 1964 KiB  
Review
Oxidative-Signaling in Neural Stem Cell-Mediated Plasticity: Implications for Neurodegenerative Diseases
by Mafalda Ferreira dos Santos, Catarina Roxo and Susana Solá
Antioxidants 2021, 10(7), 1088; https://doi.org/10.3390/antiox10071088 - 06 Jul 2021
Cited by 7 | Viewed by 3598
Abstract
The adult mammalian brain is capable of generating new neurons from existing neural stem cells (NSCs) in a process called adult neurogenesis. This process, which is critical for sustaining cognition and mental health in the mature brain, can be severely hampered with ageing [...] Read more.
The adult mammalian brain is capable of generating new neurons from existing neural stem cells (NSCs) in a process called adult neurogenesis. This process, which is critical for sustaining cognition and mental health in the mature brain, can be severely hampered with ageing and different neurological disorders. Recently, it is believed that the beneficial effects of NSCs in the injured brain relies not only on their potential to differentiate and integrate into the preexisting network, but also on their secreted molecules. In fact, further insight into adult NSC function is being gained, pointing to these cells as powerful endogenous “factories” that produce and secrete a large range of bioactive molecules with therapeutic properties. Beyond anti-inflammatory, neurogenic and neurotrophic effects, NSC-derived secretome has antioxidant proprieties that prevent mitochondrial dysfunction and rescue recipient cells from oxidative damage. This is particularly important in neurodegenerative contexts, where oxidative stress and mitochondrial dysfunction play a significant role. In this review, we discuss the current knowledge and the therapeutic opportunities of NSC secretome for neurodegenerative diseases with a particular focus on mitochondria and its oxidative state. Full article
(This article belongs to the Special Issue Mitochondrial Metabolism in Neural Regeneration)
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