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Biomolecules
Special Issues
Mitochondria and Central Nervous System Disorders: 3rd Edition
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Mitochondria and Central Nervous System Disorders: 3rd Edition

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: 30 April 2026 | Viewed by 6880

Special Issue Editors

Dr. Marta Zaninello

E-Mail Website
Guest Editor
1. Institute of Human Genetics, University of Cologne, Cologne, Germany
2. Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases, University of Cologne, Cologne, Germany
Interests: mitochondria; translation; autophagy; neurons
Special Issues, Collections and Topics in MDPI journals
Dr. Camilla Bean

E-Mail Website
Guest Editor
Department of Medicine, University of Udine, 33100 Udine, Italy
Interests: mitochondria; metabolism; transcriptomics; epigenetics
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Following the success of the previous Special Issues, we are pleased to announce the launch of a third edition, “Mitochondria and Central Nervous System Disorders: 3rd Edition”.

In the past several decades, a mitochondria-centric vision has developed in the fields of cell, organ, and organismal physiology, demonstrating exponential growth. This is likely due to the number of findings highlighting the contribution of these organelles to cell/tissue bioenergetics, death programmes, and metabolism. Dysfunctional mitochondria or dysfunctional mitochondria dynamics (a term that includes processes dictating the morphology of these organelles, their subcellular distribution/transport, or their interaction with other organelles, consequently influencing their function) have been linked to many pathological conditions, widespread among the entire human body. However, these alterations appear to more strongly affect the highly specialized and delicate cells of the central nervous system (CNS), contributing to the onset of a variety of diseases, ranging from rare childhood disorders (e.g., Leigh syndrome or mitochondrial encephalopathy with lactic acidosis and stroke-like episodes) to more common age-related neurodegenerative conditions (e.g., dementia, Alzheimer’s disease, and Parkinson’s disease).

This Special Issue is designed to emphasize the link between the (dys)function of mitochondria and CNS disorders, likely highlighting common or discrepant mechanisms underlying them. In this regard, we would like to invite review articles that address the above-mentioned topics or original research papers providing new evidence on the mitochondria–CNS pathological connection.

We look forward to reading your contributions.

Dr. Marta Zaninello
Dr. Camilla Bean
Guest Editors

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. Biomolecules 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 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
  • metabolism
  • neurodegeneration
  • neuroinflammation
  • ageing
  • central nervous system

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Published Papers (5 papers)

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Research

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14 pages, 1711 KB  
Article
A De Novo DNM1L Mutation in Twins with Variable Symptoms, Including Paraparesis and Optic Neuropathy
by Alessia Nasca, Alessia Catania, Andrea Legati, Rossella Izzo, Carola D’onofrio, Teresa Ciavattini, Eleonora Lamantea, Costanza Lamperti and Daniele Ghezzi
Biomolecules 2025, 15(9), 1230; https://doi.org/10.3390/biom15091230 - 26 Aug 2025
Viewed by 435
Abstract
Mitochondrial network dynamics, encompassing processes like fission, fusion, and mitophagy, are crucial for mitochondrial function and overall cellular health. Dysregulation of these processes has been linked to various human diseases. Particularly, pathogenic variants in the gene DNM1L can lead to a broad range [...] Read more.
Mitochondrial network dynamics, encompassing processes like fission, fusion, and mitophagy, are crucial for mitochondrial function and overall cellular health. Dysregulation of these processes has been linked to various human diseases. Particularly, pathogenic variants in the gene DNM1L can lead to a broad range of clinical phenotypes, ranging from isolated optic atrophy to severe neurological conditions. DNM1L encodes DRP1 (dynamin-1-like protein), which is a key player in mitochondrial and peroxisomal fission. This study describes two twin sisters with a de novo heterozygous variant in DNM1L, due to possible paternal germline mosaicism identified through clinical exome sequencing. The two twins showed a variable clinical presentation, including paraparesis and optic neuropathy. Functional studies of patient-derived fibroblasts revealed altered mitochondrial and peroxisomal morphology, along with dysregulated DNM1L transcript levels, indicating the deleterious effect of the variant. These findings allowed us to reclassify the identified variant from a variant of uncertain significance to a likely pathogenic variant. Our report provides insight into the phenotypic spectrum of DNM1L-related disorders and highlights the need to combine genetic and functional analyses to accurately diagnose rare mitochondrial diseases. Full article
(This article belongs to the Special Issue Mitochondria and Central Nervous System Disorders: 3rd Edition)
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18 pages, 3494 KB  
Article
Remodeling of Mitochondria–Endoplasmic Reticulum Contact Sites Accompanies LUHMES Differentiation
by Emad Norouzi Esfahani, Tomas Knedlik, Sang Hun Shin, Ana Paula Magalhães Rebelo, Agnese De Mario, Caterina Vianello, Luca Persano, Elena Rampazzo, Paolo Edomi, Camilla Bean, Dario Brunetti, Luca Scorrano, Samuele Greco, Marco Gerdol and Marta Giacomello
Biomolecules 2025, 15(1), 126; https://doi.org/10.3390/biom15010126 - 14 Jan 2025
Viewed by 1611
Abstract
Neural progenitor cells (NPCs) are often used to study the subcellular mechanisms underlying differentiation into neurons in vitro. Works published to date have focused on the pathways that distinguish undifferentiated NPCs from mature neurons, neglecting the earlier and intermediate stages of this process. [...] Read more.
Neural progenitor cells (NPCs) are often used to study the subcellular mechanisms underlying differentiation into neurons in vitro. Works published to date have focused on the pathways that distinguish undifferentiated NPCs from mature neurons, neglecting the earlier and intermediate stages of this process. Current evidence suggests that mitochondria interaction with the ER is fundamental to a wide range of intracellular processes. However, it is not clear whether and how the mitochondria–ER interactions differ between NPCs and their differentiated counterparts. Here we take advantage of the widely used NPC line LUHMES to provide hints on the mitochondrial dynamic trait changes that occur during the first stage of their maturation into dopaminergic-like neurons. We observed that the morphology of mitochondria, their interaction with the ER, and the expression of several mitochondria–ER contact site resident proteins change, which suggests the potential contribution of mitochondria dynamics to NPC differentiation. Further studies will be needed to explore in depth these changes, and their functional outcomes, which may be relevant to the scientific community focusing on embryonic neurogenesis and developmental neurotoxicity. Full article
(This article belongs to the Special Issue Mitochondria and Central Nervous System Disorders: 3rd Edition)
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Review

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32 pages, 1220 KB  
Review
Mitochondrial Aging in the CNS: Unravelling Implications for Neurological Health and Disease
by Davide Steffan, Camilla Pezzini, Martina Esposito and Anais Franco-Romero
Biomolecules 2025, 15(9), 1252; https://doi.org/10.3390/biom15091252 - 29 Aug 2025
Viewed by 696
Abstract
Mitochondrial aging plays a central role in the functional decline of the central nervous system (CNS), with profound consequences for neurological health. As the brain is one of the most energy-demanding organs, neurons are particularly susceptible to mitochondrial dysfunction that arises with aging. [...] Read more.
Mitochondrial aging plays a central role in the functional decline of the central nervous system (CNS), with profound consequences for neurological health. As the brain is one of the most energy-demanding organs, neurons are particularly susceptible to mitochondrial dysfunction that arises with aging. Key features of mitochondrial aging include impaired mitochondrial dynamics, reduced mitophagy, increased production of reactive oxygen species (ROS), and accumulation of mitochondrial DNA (mtDNA) mutations. These alterations dramatically compromise neuronal bioenergetics, disrupt synaptic integrity, and promote oxidative stress and neuroinflammation, paving the path for the development of neurodegenerative diseases. This review also examines the complex mechanisms driving mitochondrial aging in the central nervous system (CNS), including the disruption of mitochondrial-organelle communication, and explores how mitochondrial dysfunction contributes to neurodegenerative diseases, such as Alzheimer’s, Parkinson’s, Huntington’s, and amyotrophic lateral sclerosis. By synthesizing current evidence and identifying key knowledge gaps, we emphasize the urgent need for targeted strategies to restore mitochondrial function, maintain cognitive health, and delay or prevent age-related neurodegeneration. Full article
(This article belongs to the Special Issue Mitochondria and Central Nervous System Disorders: 3rd Edition)
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25 pages, 1105 KB  
Review
From Obesity to Mitochondrial Dysfunction in Peripheral Tissues and in the Central Nervous System
by Francesca Marino, Lidia Petrella, Fabiano Cimmino, Amelia Pizzella, Antonietta Monda, Salvatore Allocca, Roberta Rotondo, Margherita D’Angelo, Nadia Musco, Piera Iommelli, Angela Catapano, Carmela Bagnato, Barbara Paolini and Gina Cavaliere
Biomolecules 2025, 15(5), 638; https://doi.org/10.3390/biom15050638 - 29 Apr 2025
Viewed by 1663
Abstract
Obesity is a condition of chronic low-grade inflammation affecting peripheral organs of the body, as well as the central nervous system. The adipose tissue dysfunction occurring under conditions of obesity is a key factor in the onset and progression of a variety of [...] Read more.
Obesity is a condition of chronic low-grade inflammation affecting peripheral organs of the body, as well as the central nervous system. The adipose tissue dysfunction occurring under conditions of obesity is a key factor in the onset and progression of a variety of diseases, including neurodegenerative disorders. Mitochondria, key organelles in the production of cellular energy, play an important role in this tissue dysfunction. Numerous studies highlight the close link between obesity and adipocyte mitochondrial dysfunction, resulting in excessive ROS production and adipose tissue inflammation. This inflammation is transmitted systemically, leading to metabolic disorders that also impact the central nervous system, where pro-inflammatory cytokines impair mitochondrial and cellular functions in different areas of the brain, leading to neurodegenerative diseases. To date, several bioactive compounds are able to prevent and/or slow down neurogenerative processes by acting on mitochondrial functions. Among these, some molecules present in the Mediterranean diet, such as polyphenols, carotenoids, and omega-3 PUFAs, exert a protective action due to their antioxidant and anti-inflammatory ability. The aim of this review is to provide an overview of the involvement of adipose tissue dysfunction in the development of neurodegenerative diseases including Alzheimer’s disease, Parkinson’s disease, and multiple sclerosis, emphasizing the central role played by mitochondria, the main actors in the cross-talk between adipose tissue and the central nervous system. Full article
(This article belongs to the Special Issue Mitochondria and Central Nervous System Disorders: 3rd Edition)
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17 pages, 737 KB  
Review
Mitochondrial Transplantation in Animal Models of Psychiatric Disorders: A Novel Approach to Psychiatric Treatment
by Keiko Iwata, Masafumi Noguchi and Norihito Shintani
Biomolecules 2025, 15(2), 184; https://doi.org/10.3390/biom15020184 - 27 Jan 2025
Cited by 1 | Viewed by 1558
Abstract
Mitochondria are essential for brain function, and accumulating evidence from postmortem brain studies, neuroimaging, and basic research indicates mitochondrial impairments in patients with psychiatric disorders. Restoring mitochondrial function therefore represents a promising therapeutic strategy for these conditions. Mitochondrial transplantation, an innovative approach that [...] Read more.
Mitochondria are essential for brain function, and accumulating evidence from postmortem brain studies, neuroimaging, and basic research indicates mitochondrial impairments in patients with psychiatric disorders. Restoring mitochondrial function therefore represents a promising therapeutic strategy for these conditions. Mitochondrial transplantation, an innovative approach that uses functional mitochondria to repair damaged cells, has demonstrated efficacy through various delivery methods in cell, animal, and animal disease models. This review explores the critical link between mitochondria and psychiatric disorders and provides an overview of mitochondrial transplantation as a therapeutic intervention. It highlights recent advances in mitochondrial transplantation in animal models of psychiatric disorders, focusing on delivery methods, the timing of administration, and the integration of exogenous mitochondria into brain cells. The potential therapeutic effects and the mechanisms that underlie these effects are discussed. Additionally, this review evaluates the clinical relevance, challenges, and future strategies for the application of mitochondrial transplantation in the treatment of psychiatric disorders. Full article
(This article belongs to the Special Issue Mitochondria and Central Nervous System Disorders: 3rd Edition)
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