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Molecular Mechanisms and Pathophysiology of Neuronal Aging
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Molecular Mechanisms and Pathophysiology of Neuronal Aging

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Neurobiology".

Deadline for manuscript submissions: closed (30 June 2023) | Viewed by 8658

Special Issue Editors

Prof. Dr. Dorothee Dormann

E-Mail Website
Guest Editor
1. Faculty of Biology, Institute of Molecular Physiology, Johannes Gutenberg University (JGU) Mainz, 55122 Mainz, Germany
2. Institute of Molecular Biology (IMB), 55128 Mainz, Germany
Interests: neurodegeneration; RNA-binding proteins; protein aggregation; phase separation; nucleocytoplasmic transport; post-translational modifications
Dr. Sandra Schick

E-Mail Website
Guest Editor
Chromatin Regulation Group, Institute of Molecular Biology (IMB), 55128 Mainz, Germany
Interests: chromatin and gene regulation; development and disease; BAF complexes; (epi)genomics and proteomics; molecular and cellular biology
Dr. Kristina Endres

E-Mail Website
Guest Editor
Department of Psychiatry and Psychotherapy (UM JGU), DRZUntere Zahlbacher Str. 8, 55131 Mainz, Germany
Interests: healthy aging; Alzheimer’s disease; enteric nervous system; neuroscience; secretases

Special Issue Information

Dear Colleagues,

We are delighted to announce that we are now considering submissions for a Special Issue of the International Journal of Molecular Sciences entitled “Molecular Mechanisms and Pathophysiology of Neuronal Aging”.

Aging affects nearly all living organisms—including ourselves. Neurons are particularly affected by aging, as they do not self-renew and therefore must cope with various insults accumulating within or around them over the lifetime of an organism. However, the molecular mechanisms underlying the neuronal aging process still require detailed elucidation. Moreover, there is an ongoing debate about whether aging should be considered a disease-like state or a physiological process. We welcome contributions that highlight both perspectives. All model systems are of interest, including yeast, flies, worms, fish, rodents, and humans, and articles may focus on neurons or other cell types of the central and peripheral nervous system. Topics of interest include aging-induced transcriptomic, epigenetic and proteomic changes, the role of DNA damage or proteostasis in the aging process, and the function of mitochondria or other organelles, including membrane-less organelles. However, other relevant topics will be considered, as will contributions about neurodegenerative and neuronal disorders as they relate to the aging process. Both original research articles and review papers are welcome.

Prof. Dr. Dorothee Dormann
Dr. Sandra Schick
Dr. Kristina Endres
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • neuronal aging
  • DNA damage
  • epigenetics
  • nervous system
  • proteostasis
  • neuronal disorders

Published Papers (3 papers)

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Research

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22 pages, 2814 KiB  
Article
Mitochondrial Bioenergetics, Redox Balance, and Calcium Homeostasis Dysfunction with Defective Ultrastructure and Quality Control in the Hippocampus of Aged Female C57BL/6J Mice
by Angie K. Torres, Claudia Jara, Jesús Llanquinao, Matías Lira, Daniela Cortés-Díaz and Cheril Tapia-Rojas
Int. J. Mol. Sci. 2023, 24(6), 5476; https://doi.org/10.3390/ijms24065476 - 13 Mar 2023
Cited by 4 | Viewed by 2112
Abstract
Aging is a physiological process that generates progressive decline in many cellular functions. There are many theories of aging, and one of great importance in recent years is the mitochondrial theory of aging, in which mitochondrial dysfunction that occurs at advanced age could [...] Read more.
Aging is a physiological process that generates progressive decline in many cellular functions. There are many theories of aging, and one of great importance in recent years is the mitochondrial theory of aging, in which mitochondrial dysfunction that occurs at advanced age could be responsible for the aged phenotype. In this context, there is diverse information about mitochondrial dysfunction in aging, in different models and different organs. Specifically, in the brain, different studies have shown mitochondrial dysfunction mainly in the cortex; however, until now, no study has shown all the defects in hippocampal mitochondria in aged female C57BL/6J mice. We performed a complete analysis of mitochondrial function in 3-month-old and 20-month-old (mo) female C57BL/6J mice, specifically in the hippocampus of these animals. We observed an impairment in bioenergetic function, indicated by a decrease in mitochondrial membrane potential, O2 consumption, and mitochondrial ATP production. Additionally, there was an increase in ROS production in the aged hippocampus, leading to the activation of antioxidant signaling, specifically the Nrf2 pathway. It was also observed that aged animals had deregulation of calcium homeostasis, with more sensitive mitochondria to calcium overload and deregulation of proteins related to mitochondrial dynamics and quality control processes. Finally, we observed a decrease in mitochondrial biogenesis with a decrease in mitochondrial mass and deregulation of mitophagy. These results show that during the aging process, damaged mitochondria accumulate, which could contribute to or be responsible for the aging phenotype and age-related disabilities. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Pathophysiology of Neuronal Aging)
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Review

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24 pages, 1862 KiB  
Review
Talk to Me—Interplay between Mitochondria and Microbiota in Aging
by Kristina Endres and Kristina Friedland
Int. J. Mol. Sci. 2023, 24(13), 10818; https://doi.org/10.3390/ijms241310818 - 28 Jun 2023
Cited by 1 | Viewed by 1868
Abstract
The existence of mitochondria in eukaryotic host cells as a remnant of former microbial organisms has been widely accepted, as has their fundamental role in several diseases and physiological aging. In recent years, it has become clear that the health, aging, and life [...] Read more.
The existence of mitochondria in eukaryotic host cells as a remnant of former microbial organisms has been widely accepted, as has their fundamental role in several diseases and physiological aging. In recent years, it has become clear that the health, aging, and life span of multicellular hosts are also highly dependent on the still-residing microbiota, e.g., those within the intestinal system. Due to the common evolutionary origin of mitochondria and these microbial commensals, it is intriguing to investigate if there might be a crosstalk based on preserved common properties. In the light of rising knowledge on the gut–brain axis, such crosstalk might severely affect brain homeostasis in aging, as neuronal tissue has a high energy demand and low tolerance for according functional decline. In this review, we summarize what is known about the impact of both mitochondria and the microbiome on the host’s aging process and what is known about the aging of both entities. For a long time, bacteria were assumed to be immortal; however, recent evidence indicates their aging and similar observations have been made for mitochondria. Finally, we present pathways by which mitochondria are affected by microbiota and give information about therapeutic anti-aging approaches that are based on current knowledge. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Pathophysiology of Neuronal Aging)
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23 pages, 1507 KiB  
Review
The Aging Enteric Nervous System
by Tinh Thi Nguyen, Peter Baumann, Oliver Tüscher, Sandra Schick and Kristina Endres
Int. J. Mol. Sci. 2023, 24(11), 9471; https://doi.org/10.3390/ijms24119471 - 30 May 2023
Cited by 3 | Viewed by 4276
Abstract
The gut and the brain communicate via the nervous system, hormones, microbiota-mediated substances, and the immune system. These intricate interactions have led to the term “gut-brain axis”. Unlike the brain—which is somewhat protected—the gut is exposed to a variety of factors throughout life [...] Read more.
The gut and the brain communicate via the nervous system, hormones, microbiota-mediated substances, and the immune system. These intricate interactions have led to the term “gut-brain axis”. Unlike the brain—which is somewhat protected—the gut is exposed to a variety of factors throughout life and, consequently, might be either more vulnerable or better adapted to respond to these challenges. Alterations in gut function are common in the elder population and associated with many human pathologies, including neurodegenerative diseases. Different studies suggest that changes in the nervous system of the gut, the enteric nervous system (ENS), during aging may result in gastrointestinal dysfunction and initiate human pathologies of the brain via its interconnection with the gut. This review aims at summarizing the contribution of normal cellular aging to the age-associated physiological changes of the ENS. Morphological alterations and degeneration of the aging ENS are observed in different animal models and humans, albeit with considerable variability. The aging phenotypes and pathophysiological mechanisms of the aging ENS have highlighted the involvement of enteric neurons in age-related diseases of the central nervous system such as Alzheimer’s or Parkinson’s disease. To further elucidate such mechanisms, the ENS constitutes a promising source of material for diagnosis and therapeutic predictions, as it is more accessible than the brain. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Pathophysiology of Neuronal Aging)
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