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Mitochondria: A Novel Therapeutic Target in Neurodegeneration

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

Deadline for manuscript submissions: closed (31 August 2023) | Viewed by 1927

Special Issue Editors

Prof. Dr. Jiří Neužil
E-Mail Website
Guest Editor
Institute of Biotechnology, Czech Academy of Sciences, BIOCEV, Vestec, 252 50 Prague West, Czech Republic
Interests: mitochondria
School of Pharmacy and Medical Sciences, Griffith University, Southport, QLD 4222, Australia
Interests: Parkinson's disease; multiple system atrophy; dementia with Lewy bodies; alpha-synuclein; small ubiquitin-like modifier (SUMO); metallothionein; neuroinflammation; calcium; copper; autophagy
Special Issues, Collections and Topics in MDPI journals
CNC—Center for Neuroscience and Cell Biology, CIBB—Center for Innovative Biomedicine and Biotechnology, University of Coimbra, 3004-504 Coimbra, Portugal
Interests: mitochondria; redox homeostasis; metabolism; neurodegeneration

Special Issue Information

Dear Colleagues,

Loss of neuronal function is a major hallmark of normal aging and aging-associated diseases, such as amyotrophic lateral sclerosis, Parkinson’s, Huntington’s, and Alzheimer’s Diseases, among others. Neurodegeneration can have multiple causes and manifestations, but mitochondrial dysfunction is often a common feature. Mitochondria regulate many aspects of cellular metabolism, including bioenergetics, biosynthetic pathways, calcium, and redox homeostasis. They are also involved in controlling cell survival. Thus, therapeutic strategies targeting mitochondria are promising for a wide range of conditions. Interesting processes underlying mitochondrial involvement in neurodegeneration include metabolic and redox remodeling, mitochondrial uptake of nuclear-encoded proteins, intracellular and intercellular mitochondrial dynamics, mitochondrial quality control, and interactions of pathological proteins, such as alpha-synuclein, with mitochondria. In this Special Issue, we aim to highlight mitochondrial involvement in neurodegeneration, from potential biomarkers to opportunities for intervention. Original articles, comprehensive reviews, and perspective articles are welcome.

Prof. Dr. Jiří Neužil
Dr. Dean L. Pountney
Dr. Teresa Cunha-Oliveira
Guest Editors

Manuscript Submission Information

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Keywords

  • neurodegeneration
  • mitochondrial profiling
  • redox homeostasis
  • clinical biomarkers
  • mitochondrial therapy

Published Papers (1 paper)

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Research

28 pages, 7105 KiB  
Article
Sevoflurane Exposure in Neonates Perturbs the Expression Patterns of Specific Genes That May Underly the Observed Learning and Memory Deficits
Int. J. Mol. Sci. 2023, 24(10), 8696; https://doi.org/10.3390/ijms24108696 - 12 May 2023
Cited by 1 | Viewed by 1533
Abstract
Exposure to commonly used anesthetics leads to neurotoxic effects in animal models—ranging from cell death to learning and memory deficits. These neurotoxic effects invoke a variety of molecular pathways, exerting either immediate or long-term effects at the cellular and behavioural levels. However, little [...] Read more.
Exposure to commonly used anesthetics leads to neurotoxic effects in animal models—ranging from cell death to learning and memory deficits. These neurotoxic effects invoke a variety of molecular pathways, exerting either immediate or long-term effects at the cellular and behavioural levels. However, little is known about the gene expression changes following early neonatal exposure to these anesthetic agents. We report here on the effects of sevoflurane, a commonly used inhalational anesthetic, on learning and memory and identify a key set of genes that may likely be involved in the observed behavioural deficits. Specifically, we demonstrate that sevoflurane exposure in postnatal day 7 (P7) rat pups results in subtle, but distinct, memory deficits in the adult animals that have not been reported previously. Interestingly, when given intraperitoneally, pre-treatment with dexmedetomidine (DEX) could only prevent sevoflurane-induced anxiety in open field testing. To identify genes that may have been altered in the neonatal rats after sevoflurane and DEX exposure, specifically those impacting cellular viability, learning, and memory, we conducted an extensive Nanostring study examining over 770 genes. We found differential changes in the gene expression levels after exposure to both agents. A number of the perturbed genes found in this study have previously been implicated in synaptic transmission, plasticity, neurogenesis, apoptosis, myelination, and learning and memory. Our data thus demonstrate that subtle, albeit long-term, changes observed in an adult animal’s learning and memory after neonatal anesthetic exposure may likely involve perturbation of specific gene expression patterns. Full article
(This article belongs to the Special Issue Mitochondria: A Novel Therapeutic Target in Neurodegeneration)
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