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Recent Research on the Role of Mitochondria in Neurodegeneration
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Recent Research on the Role of Mitochondria in Neurodegeneration

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cells of the Nervous System".

Deadline for manuscript submissions: 30 April 2024 | Viewed by 4190

Special Issue Editor

Dr. Kaiyin Chau

E-Mail Website
Guest Editor
Department of Clinical and Movement Neuroscience, Queens Square Institute of Neurology, University College London, London NW3 2PF, UK
Interests: molecular mechanism of neurodegeneration; mitochondrial biology; gene regulation

Special Issue Information

Dear Colleagues,

Neurodegeneration is a spectrum of diseases. The most common forms are Alzheimer’s, Parkinson's and Huntington's disease, multiple sclerosis, and amyotrophic lateral sclerosis. While neuronal loss contributes to the pathology, other cell types located in the brain including microglia and astrocytes play their roles in disease modification. Recently, the intestinal microbiome has been described as influencing brain disorders through the brain–gut axis, which illustrates the complexity of disease initiation and spread. At the molecular level, the emergence of abnormal proteins and lipids, derived from gene mutations or pathogenic processes, affects cellular physiology, and the function of organelles. Inadequate quality control and clearance of damaged lipids, proteins, and organelles exacerbate the pathogenic conditions leading to neuronal cell death. Mitochondrial alteration has been shown to be involved in multiple and key steps in neurodegeneration such as mitophagy, energy supply, calcium homeostasis, and apoptosis. This review aims to summarize some novel understanding of the role of mitochondria in mediating and protecting from neurodegeneration.

Dr. Kaiyin Chau
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. Cells is an international peer-reviewed open access semimonthly 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 2700 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

  • mitochondrial
  • neurodegeneration
  • metabolism
  • mitophagy
  • apoptosis

Published Papers (3 papers)

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Research

Jump to: Review

13 pages, 6830 KiB  
Article
Transcriptomic Analysis in the Hippocampus and Retina of Tg2576 AD Mice Reveals Defective Mitochondrial Oxidative Phosphorylation and Recovery by Tau 12A12mAb Treatment
by Giovanna Morello, Maria Guarnaccia, Valentina La Cognata, Valentina Latina, Pietro Calissano, Giuseppina Amadoro and Sebastiano Cavallaro
Cells 2023, 12(18), 2254; https://doi.org/10.3390/cells12182254 - 12 Sep 2023
Viewed by 1209
Abstract
Increasing evidence implicates decreased energy metabolism and mitochondrial dysfunctions among the earliest pathogenic events of Alzheimer’s disease (AD). However, the molecular mechanisms underlying bioenergetic dysfunctions in AD remain, to date, largely unknown. In this work, we analyzed transcriptomic changes occurring in the hippocampus [...] Read more.
Increasing evidence implicates decreased energy metabolism and mitochondrial dysfunctions among the earliest pathogenic events of Alzheimer’s disease (AD). However, the molecular mechanisms underlying bioenergetic dysfunctions in AD remain, to date, largely unknown. In this work, we analyzed transcriptomic changes occurring in the hippocampus and retina of a Tg2576 AD mouse model and wild-type controls, evaluating their functional implications by gene set enrichment analysis. The results revealed that oxidative phosphorylation and mitochondrial-related pathways are significantly down-regulated in both tissues of Tg2576 mice, supporting the role of these processes in the pathogenesis of AD. In addition, we also analyzed transcriptomic changes occurring in Tg2576 mice treated with the 12A12 monoclonal antibody that neutralizes an AD-relevant tau-derived neurotoxic peptide in vivo. Our analysis showed that the mitochondrial alterations observed in AD mice were significantly reverted by treatment with 12A12mAb, supporting bioenergetic pathways as key mediators of its in vivo neuroprotective and anti-amyloidogenic effects. This study provides, for the first time, a comprehensive characterization of molecular events underlying the disrupted mitochondrial bioenergetics in AD pathology, laying the foundation for the future development of diagnostic and therapeutic tools. Full article
(This article belongs to the Special Issue Recent Research on the Role of Mitochondria in Neurodegeneration)
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17 pages, 3613 KiB  
Article
Metabolic Alterations Caused by Simultaneous Loss of HK2 and PKM2 Leads to Photoreceptor Dysfunction and Degeneration
by Eric Weh, Moloy Goswami, Sraboni Chaudhury, Roshini Fernando, Nick Miller, Heather Hager, Sarah Sheskey, Vikram Sharma, Thomas J. Wubben and Cagri G. Besirli
Cells 2023, 12(16), 2043; https://doi.org/10.3390/cells12162043 - 10 Aug 2023
Cited by 1 | Viewed by 1158
Abstract
HK2 and PKM2 are two main regulators of aerobic glycolysis. Photoreceptors (PRs) use aerobic glycolysis to produce the biomass necessary for the daily renewal of their outer segments. Previous work has shown that HK2 and PKM2 are important for the normal function and [...] Read more.
HK2 and PKM2 are two main regulators of aerobic glycolysis. Photoreceptors (PRs) use aerobic glycolysis to produce the biomass necessary for the daily renewal of their outer segments. Previous work has shown that HK2 and PKM2 are important for the normal function and long-term survival of PRs but are dispensable for PR maturation, and their individual loss has opposing effects on PR survival during acute nutrient deprivation. We generated double conditional (dcKO) mice lacking HK2 and PKM2 expression in rod PRs. Western blotting, immunofluorescence, optical coherence tomography, and electroretinography were used to characterize the phenotype of dcKO animals. Targeted and stable isotope tracing metabolomics, qRT-PCR, and retinal oxygen consumption were performed. We show that dcKO animals displayed early shortening of PR inner/outer segments, followed by loss of PRs with aging, much more rapidly than either knockout alone without functional loss as measured by ERG. Significant alterations to central glucose metabolism were observed without any apparent changes to mitochondrial function, prior to PR degeneration. Finally, PR survival following experimental retinal detachment was unchanged in dcKO animals as compared to wild-type animals. These data suggest that HK2 and PKM2 have differing roles in promoting PR neuroprotection and identifying them has important implications for developing therapeutic options for combating PR loss during retinal disease. Full article
(This article belongs to the Special Issue Recent Research on the Role of Mitochondria in Neurodegeneration)
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Review

Jump to: Research

24 pages, 6660 KiB  
Review
The Role of Mitophagy in Glaucomatous Neurodegeneration
by Dimitrios Stavropoulos, Manjot K. Grewal, Bledi Petriti, Kai-Yin Chau, Christopher J. Hammond, David F. Garway-Heath and Gerassimos Lascaratos
Cells 2023, 12(15), 1969; https://doi.org/10.3390/cells12151969 - 30 Jul 2023
Viewed by 1452
Abstract
This review aims to provide a better understanding of the emerging role of mitophagy in glaucomatous neurodegeneration, which is the primary cause of irreversible blindness worldwide. Increasing evidence from genetic and other experimental studies suggests that mitophagy-related genes are implicated in the pathogenesis [...] Read more.
This review aims to provide a better understanding of the emerging role of mitophagy in glaucomatous neurodegeneration, which is the primary cause of irreversible blindness worldwide. Increasing evidence from genetic and other experimental studies suggests that mitophagy-related genes are implicated in the pathogenesis of glaucoma in various populations. The association between polymorphisms in these genes and increased risk of glaucoma is presented. Reduction in intraocular pressure (IOP) is currently the only modifiable risk factor for glaucoma, while clinical trials highlight the inadequacy of IOP-lowering therapeutic approaches to prevent sight loss in many glaucoma patients. Mitochondrial dysfunction is thought to increase the susceptibility of retinal ganglion cells (RGCs) to other risk factors and is implicated in glaucomatous degeneration. Mitophagy holds a vital role in mitochondrial quality control processes, and the current review explores the mitophagy-related pathways which may be linked to glaucoma and their therapeutic potential. Full article
(This article belongs to the Special Issue Recent Research on the Role of Mitochondria in Neurodegeneration)
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