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Cells
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Mitochondria in Developmental and Age-Associated Neurodegenerative Diseases
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Mitochondria in Developmental and Age-Associated Neurodegenerative Diseases

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

Deadline for manuscript submissions: closed (31 December 2023) | Viewed by 3363

Special Issue Editor

Dr. Sarah Annesley

E-Mail Website
Guest Editor
Department of Physiology, Anatomy and Microbiology, La Trobe University, Bundoora, VIC 3086, Australia
Interests: mitochondria; neurodegenerative disease; Parkinson’s disease; myalgic encephalomyelitis/chronic fatigue syndrome; long COVID; Dictyostelium discoideum
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Neurodegenerative diseases are a diverse group of disorders that are characterized by the progressive degeneration and subsequent death of neurons in specific areas of the brain. Many of these are associated with aging, such as Alzheimer’s and Parkinson’s diseases, but there are also a large number that are associated with development; these occur in childhood  and include Friedreich Ataxia and Batten diseases. Whilst the underlying disease pathways have not yet been clearly defined, mitochondrial function has been recognized as a central player. In addition to producing over 90% of cell energy, mitochondria are integral in key cellular processes, including iron and calcium homeostasis, cell death, aging, and cell development.

This Special Issue focuses on all aspects of mitochondrial function in childhood neurodegenerative diseases and those associated with aging. In recognition of the contributions that diverse models have made to our understanding of these disorders, this Special Issue encourages the submission of papers from research using simple model organisms, cellular models, and animal models. Both review articles and original research papers are welcome.

Dr. Sarah Annesley
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

  • mitochondria
  • neurodegenerative disease
  • mitochondrial biogenesis
  • calcium signaling
  • ROS production
  • cell death
  • Parkinson’s disease
  • Alzheimer’s disease
  • Batten disease
  • Friedreich’s Ataxia

Published Papers (2 papers)

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Research

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25 pages, 3357 KiB  
Article
Genetically Engineered Triple MAPT-Mutant Human-Induced Pluripotent Stem Cells (N279K, P301L, and E10+16 Mutations) Exhibit Impairments in Mitochondrial Bioenergetics and Dynamics
by Leonora Szabo, Amandine Grimm, Juan Antonio García-León, Catherine M. Verfaillie and Anne Eckert
Cells 2023, 12(10), 1385; https://doi.org/10.3390/cells12101385 - 13 May 2023
Cited by 1 | Viewed by 2067
Abstract
Pathological abnormalities in the tau protein give rise to a variety of neurodegenerative diseases, conjointly termed tauopathies. Several tau mutations have been identified in the tau-encoding gene MAPT, affecting either the physical properties of tau or resulting in altered tau splicing. At [...] Read more.
Pathological abnormalities in the tau protein give rise to a variety of neurodegenerative diseases, conjointly termed tauopathies. Several tau mutations have been identified in the tau-encoding gene MAPT, affecting either the physical properties of tau or resulting in altered tau splicing. At early disease stages, mitochondrial dysfunction was highlighted with mutant tau compromising almost every aspect of mitochondrial function. Additionally, mitochondria have emerged as fundamental regulators of stem cell function. Here, we show that compared to the isogenic wild-type triple MAPT-mutant human-induced pluripotent stem cells, bearing the pathogenic N279K, P301L, and E10+16 mutations, exhibit deficits in mitochondrial bioenergetics and present altered parameters linked to the metabolic regulation of mitochondria. Moreover, we demonstrate that the triple tau mutations disturb the cellular redox homeostasis and modify the mitochondrial network morphology and distribution. This study provides the first characterization of disease-associated tau-mediated mitochondrial impairments in an advanced human cellular tau pathology model at early disease stages, ranging from mitochondrial bioenergetics to dynamics. Consequently, comprehending better the influence of dysfunctional mitochondria on the development and differentiation of stem cells and their contribution to disease progression may thus assist in the potential prevention and treatment of tau-related neurodegeneration. Full article
(This article belongs to the Special Issue Mitochondria in Developmental and Age-Associated Neurodegenerative Diseases)
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Review

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18 pages, 1505 KiB  
Review
The Role of Cardiolipin in Mitochondrial Function and Neurodegenerative Diseases
by José M. Fuentes and Patricia Morcillo
Cells 2024, 13(7), 609; https://doi.org/10.3390/cells13070609 - 30 Mar 2024
Viewed by 986
Abstract
Cardiolipin (CL) is a mitochondria-exclusive phospholipid synthesized in the inner mitochondrial membrane. CL plays a key role in mitochondrial membranes, impacting a plethora of functions this organelle performs. Consequently, it is conceivable that abnormalities in the CL content, composition, and level of oxidation [...] Read more.
Cardiolipin (CL) is a mitochondria-exclusive phospholipid synthesized in the inner mitochondrial membrane. CL plays a key role in mitochondrial membranes, impacting a plethora of functions this organelle performs. Consequently, it is conceivable that abnormalities in the CL content, composition, and level of oxidation may negatively impact mitochondrial function and dynamics, with important implications in a variety of diseases. This review concentrates on papers published in recent years, combined with basic and underexplored research in CL. We capture new findings on its biological functions in the mitochondria, as well as its association with neurodegenerative diseases such as Alzheimer’s disease or Parkinson’s disease. Lastly, we explore the potential applications of CL as a biomarker and pharmacological target to mitigate mitochondrial dysfunction. Full article
(This article belongs to the Special Issue Mitochondria in Developmental and Age-Associated Neurodegenerative Diseases)
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