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Biomedicines
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Mitochondria and Brain Disease 2.0
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Mitochondria and Brain Disease 2.0

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Neurobiology and Clinical Neuroscience".

Deadline for manuscript submissions: closed (31 August 2023) | Viewed by 20414

Special Issue Editor

Dr. Susana Cardoso

E-Mail Website
Guest Editor
Center for Neuroscience and Cell Biology, University of Coimbra, 3004-504 Coimbra, Portugal
Interests: diabetes; Alzheimer´s disease; mental disorders; mitochondria; oxidative stress; uncoupling proteins; brain metabolism
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Brain diseases, which can come in different forms (e.g., traumatic brain injuries, strokes, seizures, mental illnesses, dementia, neurodegenerative disorders), are a significant global health issue. The World Health Organization (WHO) estimates that over a billion people worldwide are affected with one neurological or mental health debilitating condition. In the past few decades, research in brain pathologies has made great progress in clarifying the pathophysiological mechanisms contributing to disease appearance and progress. Among these, impaired mitochondrial function has taken center stage as a causative factor in brain disease pathogenesis. Apart from being a primary metabolic platform for brain cells, mitochondrial biological activities also include several other processes like calcium homeostasis, reactive oxygen species (ROS) neutralization, amino-acid metabolism, neurotransmission and plasticity etc. As the world is moving into a new era of mitochondrial medicine, foci of current research include providing feasible strategies to directly manage the major insidious disturbances of mitochondrial homeostasis as well as attempts to directly or indirectly manage its consequences in the context of brain disease. After a successful first edition of “Mitochondria and Brain Disease”, we are pleased to announce the second volume of this Special Issue. Herein, we intend to guide readers through the multifaceted investigation of mitochondrial function and mitochondria-directed interventions in the broad and heterogeneous field of brain diseases. For that, this volume “Mitochondria and Brain Disease 2.0” invites authors to contribute to this area of research with either original research articles or comprehensive literature reviews.

Dr. Susana Cardoso
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. Biomedicines 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 2600 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

  • brain injury
  • dementia
  • mental health
  • metabolism
  • mitochondria
  • mitochondrial medicine
  • neurodegenerative disorders
  • oxidative stress
  • stroke
  • translational medicine

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Published Papers (5 papers)

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Research

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21 pages, 1989 KiB  
Article
HMTM-Mediated Enhancement of Brain Bioenergetics in a Mouse Tauopathy Model Is Blocked by Chronic Administration of Rivastigmine
by Renato X. Santos, Valeria Melis, Elizabeth A. Goatman, Michael Leith, Thomas C. Baddeley, John M. D. Storey, Gernot Riedel, Claude M. Wischik and Charles R. Harrington
Biomedicines 2022, 10(4), 867; https://doi.org/10.3390/biomedicines10040867 - 07 Apr 2022
Cited by 1 | Viewed by 2669
Abstract
The tau protein aggregation inhibitor hydromethylthionine mesylate (HMTM) was shown recently to have concentration-dependent pharmacological activity in delaying cognitive decline and brain atrophy in phase 3 Alzheimer’s disease (AD) clinical trials; the activity was reduced in patients receiving symptomatic therapies. The methylthionine (MT) [...] Read more.
The tau protein aggregation inhibitor hydromethylthionine mesylate (HMTM) was shown recently to have concentration-dependent pharmacological activity in delaying cognitive decline and brain atrophy in phase 3 Alzheimer’s disease (AD) clinical trials; the activity was reduced in patients receiving symptomatic therapies. The methylthionine (MT) moiety has been reported to increase the clearance of pathological tau and to enhance mitochondrial activity, which is impaired in AD patients. In line 1 (L1) mice (a model of AD), HMTM (5/15 mg/kg) was administered either as a monotherapy or as an add-on to a chronic administration with the cholinesterase inhibitor rivastigmine (0.1/0.5 mg/kg) to explore mitochondrial function and energy substrate utilization as potential targets of drug interference. Compared with wild-type NMRI mice, the L1 mice accumulated greater levels of l-lactate and of the LDH-A subunit responsible for the conversion of pyruvate into l-lactate. In contrast, the levels of LDH-B and mitochondrial ETC subunits and the activity of complexes I and IV was not altered in the L1 mice. The activity of complex I and complex IV tended to increase with the HMTM dosing, in turn decreasing l-lactate accumulation in the brains of the L1 mice, despite increasing the levels of LDH-A. The chronic pre-dosing of the L1 mice with rivastigmine partially prevented the enhancement of the activity of complexes I and IV by HMTM and the increase in the levels of LDH-A while further reducing the levels of l-lactate. Thus, HMTM in combination with rivastigmine leads to a depletion in the energy substrate l-lactate, despite bioenergetic production not being favoured. In this study, the changes in l-lactate appear to be regulated by LDH-A, since neither of the experimental conditions affected the levels of LDH-B. The data show that HMTM monotherapy facilitates the use of substrates for energy production, particularly l-lactate, which is provided by astrocytes, additionally demonstrating that a chronic pre-treatment with rivastigmine prevented most of the HMTM-associated effects. Full article
(This article belongs to the Special Issue Mitochondria and Brain Disease 2.0)
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Review

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52 pages, 2123 KiB  
Review
Mitochondria and Brain Disease: A Comprehensive Review of Pathological Mechanisms and Therapeutic Opportunities
by Vicente Javier Clemente-Suárez, Laura Redondo-Flórez, Ana Isabel Beltrán-Velasco, Domingo Jesús Ramos-Campo, Pedro Belinchón-deMiguel, Ismael Martinez-Guardado, Athanasios A. Dalamitros, Rodrigo Yáñez-Sepúlveda, Alexandra Martín-Rodríguez and José Francisco Tornero-Aguilera
Biomedicines 2023, 11(9), 2488; https://doi.org/10.3390/biomedicines11092488 - 07 Sep 2023
Cited by 7 | Viewed by 4765
Abstract
Mitochondria play a vital role in maintaining cellular energy homeostasis, regulating apoptosis, and controlling redox signaling. Dysfunction of mitochondria has been implicated in the pathogenesis of various brain diseases, including neurodegenerative disorders, stroke, and psychiatric illnesses. This review paper provides a comprehensive overview [...] Read more.
Mitochondria play a vital role in maintaining cellular energy homeostasis, regulating apoptosis, and controlling redox signaling. Dysfunction of mitochondria has been implicated in the pathogenesis of various brain diseases, including neurodegenerative disorders, stroke, and psychiatric illnesses. This review paper provides a comprehensive overview of the intricate relationship between mitochondria and brain disease, focusing on the underlying pathological mechanisms and exploring potential therapeutic opportunities. The review covers key topics such as mitochondrial DNA mutations, impaired oxidative phosphorylation, mitochondrial dynamics, calcium dysregulation, and reactive oxygen species generation in the context of brain disease. Additionally, it discusses emerging strategies targeting mitochondrial dysfunction, including mitochondrial protective agents, metabolic modulators, and gene therapy approaches. By critically analysing the existing literature and recent advancements, this review aims to enhance our understanding of the multifaceted role of mitochondria in brain disease and shed light on novel therapeutic interventions. Full article
(This article belongs to the Special Issue Mitochondria and Brain Disease 2.0)
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21 pages, 1272 KiB  
Review
Mitochondrial Ca2+ Signaling and Bioenergetics in Alzheimer’s Disease
by Nikita Arnst, Nelly Redolfi, Annamaria Lia, Martina Bedetta, Elisa Greotti and Paola Pizzo
Biomedicines 2022, 10(12), 3025; https://doi.org/10.3390/biomedicines10123025 - 24 Nov 2022
Cited by 6 | Viewed by 2514
Abstract
Alzheimer’s disease (AD) is a hereditary and sporadic neurodegenerative illness defined by the gradual and cumulative loss of neurons in specific brain areas. The processes that cause AD are still under investigation and there are no available therapies to halt it. Current progress [...] Read more.
Alzheimer’s disease (AD) is a hereditary and sporadic neurodegenerative illness defined by the gradual and cumulative loss of neurons in specific brain areas. The processes that cause AD are still under investigation and there are no available therapies to halt it. Current progress puts at the forefront the “calcium (Ca2+) hypothesis” as a key AD pathogenic pathway, impacting neuronal, astrocyte and microglial function. In this review, we focused on mitochondrial Ca2+ alterations in AD, their causes and bioenergetic consequences in neuronal and glial cells, summarizing the possible mechanisms linking detrimental mitochondrial Ca2+ signals to neuronal death in different experimental AD models. Full article
(This article belongs to the Special Issue Mitochondria and Brain Disease 2.0)
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19 pages, 1133 KiB  
Review
Activation of the Mitochondrial Unfolded Protein Response: A New Therapeutic Target?
by Juan M. Suárez-Rivero, Carmen J. Pastor-Maldonado, Suleva Povea-Cabello, Mónica Álvarez-Córdoba, Irene Villalón-García, Marta Talaverón-Rey, Alejandra Suárez-Carrillo, Manuel Munuera-Cabeza, Diana Reche-López, Paula Cilleros-Holgado, Rocío Piñero-Pérez and José A. Sánchez-Alcázar
Biomedicines 2022, 10(7), 1611; https://doi.org/10.3390/biomedicines10071611 - 06 Jul 2022
Cited by 16 | Viewed by 4062
Abstract
Mitochondrial dysfunction is a key hub that is common to many diseases. Mitochondria’s role in energy production, calcium homeostasis, and ROS balance makes them essential for cell survival and fitness. However, there are no effective treatments for most mitochondrial and related diseases to [...] Read more.
Mitochondrial dysfunction is a key hub that is common to many diseases. Mitochondria’s role in energy production, calcium homeostasis, and ROS balance makes them essential for cell survival and fitness. However, there are no effective treatments for most mitochondrial and related diseases to this day. Therefore, new therapeutic approaches, such as activation of the mitochondrial unfolded protein response (UPRmt), are being examined. UPRmt englobes several compensation processes related to proteostasis and antioxidant mechanisms. UPRmt activation, through an hormetic response, promotes cell homeostasis and improves lifespan and disease conditions in biological models of neurodegenerative diseases, cardiopathies, and mitochondrial diseases. Although UPRmt activation is a promising therapeutic option for many conditions, its overactivation could lead to non-desired side effects, such as increased heteroplasmy of mitochondrial DNA mutations or cancer progression in oncologic patients. In this review, we present the most recent UPRmt activation therapeutic strategies, UPRmt’s role in diseases, and its possible negative consequences in particular pathological conditions. Full article
(This article belongs to the Special Issue Mitochondria and Brain Disease 2.0)
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26 pages, 1901 KiB  
Review
Oxidative Stress in Ischemia/Reperfusion Injuries following Acute Ischemic Stroke
by Anamaria Jurcau and Adriana Ioana Ardelean
Biomedicines 2022, 10(3), 574; https://doi.org/10.3390/biomedicines10030574 - 01 Mar 2022
Cited by 50 | Viewed by 5420
Abstract
Recanalization therapy is increasingly used in the treatment of acute ischemic stroke. However, in about one third of these patients, recanalization is followed by ischemia/reperfusion injuries, and clinically to worsening of the neurological status. Much research has focused on unraveling the involved mechanisms [...] Read more.
Recanalization therapy is increasingly used in the treatment of acute ischemic stroke. However, in about one third of these patients, recanalization is followed by ischemia/reperfusion injuries, and clinically to worsening of the neurological status. Much research has focused on unraveling the involved mechanisms in order to prevent or efficiently treat these injuries. What we know so far is that oxidative stress and mitochondrial dysfunction are significantly involved in the pathogenesis of ischemia/reperfusion injury. However, despite promising results obtained in experimental research, clinical studies trying to interfere with the oxidative pathways have mostly failed. The current article discusses the main mechanisms leading to ischemia/reperfusion injuries, such as mitochondrial dysfunction, excitotoxicity, and oxidative stress, and reviews the clinical trials with antioxidant molecules highlighting recent developments and future strategies. Full article
(This article belongs to the Special Issue Mitochondria and Brain Disease 2.0)
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