Mitochondrial Dysfunctions: A Red Thread across Neurodegenerative Diseases.

Int J Mol Sci

Department of Neuroscience Rita Levi Montalcini, University of Turin, 10126 Turin, Italy.

Published: May 2020

Mitochondria play a central role in a plethora of processes related to the maintenance of cellular homeostasis and genomic integrity. They contribute to preserving the optimal functioning of cells and protecting them from potential DNA damage which could result in mutations and disease. However, perturbations of the system due to senescence or environmental factors induce alterations of the physiological balance and lead to the impairment of mitochondrial functions. After the description of the crucial roles of mitochondria for cell survival and activity, the core of this review focuses on the "mitochondrial switch" which occurs at the onset of neuronal degeneration. We dissect the pathways related to mitochondrial dysfunctions which are shared among the most frequent or disabling neurodegenerative diseases such as Alzheimer's, Parkinson's, and Huntington's, Amyotrophic Lateral Sclerosis, and Spinal Muscular Atrophy. Can mitochondrial dysfunctions (affecting their morphology and activities) represent the early event eliciting the shift towards pathological neurobiological processes? Can mitochondria represent a common target against neurodegeneration? We also review here the drugs that target mitochondria in neurodegenerative diseases.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7279270PMC
http://dx.doi.org/10.3390/ijms21103719DOI Listing

Publication Analysis

Top Keywords

mitochondrial dysfunctions
12
neurodegenerative diseases
12
mitochondrial
4
dysfunctions red
4
red thread
4
thread neurodegenerative
4
mitochondria
4
diseases mitochondria
4
mitochondria play
4
play central
4

Similar Publications

Nonantibiotic strategies are urgently needed to treat acute drug-resistant bacterial pneumonia. Recently, nanomaterial-mediated bacterial cuproptosis has arisen widespread interest due to its superiority against antibiotic resistance. However, it may also cause indiscriminate and irreversible damage to healthy cells.

View Article and Find Full Text PDF

Exploring ferroptosis and miRNAs: implications for cancer modulation and therapy.

Mol Cell Biochem

January 2025

Department of Molecular Genetics, Faculty of Biological Sciences, Tarbiat Modares University, P.O. Box: 14115-154, Tehran, Iran.

Ferroptosis is a novel, iron-dependent form of non-apoptotic cell death characterized by the accumulation of lipid reactive oxygen species (ROS) and mitochondrial shrinkage. It is closely associated with the onset and progression of various diseases, especially cancer, at all stages, making it a key focus of research for developing therapeutic strategies. Numerous studies have explored the role of microRNAs (miRNAs) in regulating ferroptosis by modulating the expression of critical genes involved in iron metabolism and lipid peroxidation.

View Article and Find Full Text PDF

The complete genome sequence of , a goldthread anthracnose pathogen, was sequenced using PacBio Revio and MGI DNBSEQ-T7 PE150. It contains 10 chromosomes, 5 mini chromosomes, a circular mitochondrial chromosome, and 13,129 genes predicted with RNA-Seq data in a 52.13-Mb genome with an of 5.

View Article and Find Full Text PDF

The polymerase gamma (POLG) gene mutation is associated with mitochondria and metabolism disorders, resulting in heterogeneous responses to immunological activation and posing challenges for mitochondrial disease therapy. Optical metabolic imaging captures the autofluorescent signal of two coenzymes, NADH and FAD, and offers a label-free approach to detect cellular metabolic phenotypes, track mitochondria morphology, and quantify metabolic heterogeneity. In this study, fluorescence lifetime imaging (FLIM) of NAD(P)H and FAD revealed that POLG mutator macrophages exhibit a decreased NAD(P)H lifetime, and optical redox ratio compared to the wild-type macrophages, indicating an increased dependence on glycolysis.

View Article and Find Full Text PDF

Potassium channels regulate membrane potential, calcium flux, cellular activation and effector functions of adaptive and innate immune cells. The voltage-activated Kv1.3 channel is an important regulator of T cell-mediated autoimmunity and microglia-mediated neuroinflammation.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!