Oxidative Medicine and Cellular Longevity

Mitochondrial Dysfunction and Oxidative Stress in Neurodegeneration


Publishing date
01 Jul 2022
Status
Closed
Submission deadline
25 Feb 2022

1Novel Global Community Educational Foundation, Hebersham, Australia

2University of Milano-Bicocca, Milan, Italy

3Sichuan University, Chengdu, China

This issue is now closed for submissions.
More articles will be published in the near future.

Mitochondrial Dysfunction and Oxidative Stress in Neurodegeneration

This issue is now closed for submissions.
More articles will be published in the near future.

Description

Several pathophysiological factors are implicated in neurodegeneration, including but not limited to protein misfolding, dysfunction and aggregation of the proteasome, mutations of molecular chaperones, oxidative stress and formation of free radicals or reactive oxygen species (ROS), mitochondrial dysfunction, and neuroinflammation. Mitochondria are involved in the maintenance of calcium homeostasis, inorganic cofactor iron-sulfur clusters, ROS generation, and signaling and metabolism of lipids, in close association with the endoplasmic reticulum. Moreover, they are a primary contributor to amyloid and tau deposition in brain tissue in Alzheimer’s disease. Dopaminergic neurons, cholinergic receptors, and numerous structures involved in neurodegeneration are prone to oxidative stress, which invokes a cascade of events, including mitochondrial dysfunction and neuroinflammation. Therefore, the impairment of nuclear and mtDNA contributes to the degradation of neurons and subsequent clinical effects.

Many correlated or uncorrelated factors can disturb mitochondrial morphology and alter mitochondrial dynamics, resulting in electrophysiology problems correlated with neurodegenerative disorders. Continuous changes by fission and fusion events can lead to an irreversible loss of internal mitochondrial structural features, limiting the internal area and energy and promoting apoptosis. In deficient infusion cells, the large mesh of interconnected mitochondria prohibits efficient mitochondrial motility in small pathways like neuronal processes. However, the cause of this decreased mitochondrial motility in fusion deficient cells is not very clear. Additionally, mtDNA accumulates mutations at a much higher rate than nuclear DNA, mostly because of higher replication rates and less efficient repair mechanisms, leading to the formation of SNPs. Comparative analysis of very large worldwide mtDNA SNP datasets has led to the classification of human mtDNA into certain groupings known as mtDNA haplogroups, reflecting maternal ancestral lineages with specific phylogeographic distributions. Significant effort has been put into connecting mtDNA haplogroups with the risk of neurodegeneration.

Limitations in mitochondrial bioenergetics and oxidative phosphorylation are often associated with increased free radical production and consequently oxidative damage that may contribute to neurodegenerative diseases. Therefore, this Special Issue aims to collate innovative original research and review articles that reveal pathogenic pathways and potential therapeutic targets, presenting the crosstalk between oxidative stress and mitochondrial dynamics.

Potential topics include but are not limited to the following:

  • Evidence of mitochondrial dysfunction and regional alterations of brain metabolism and their relation to other somatic symptoms
  • Mitochondrial dynamics in neurodegeneration
  • Methods, protocols, and computational tools for mitochondrial testing in neurodegeneration
  • Novel therapies addressing mitochondrial dysfunction and oxidative stress
  • Signs and lesions of mitochondrial dysfunctionalities in early or moderate mild cognitive impairment (MCI)
  • SNP formation and mtDNA haplogroups

Articles

  • Special Issue
  • - Volume 2022
  • - Article ID 5641727
  • - Research Article

Segmentation of Drug-Treated Cell Image and Mitochondrial-Oxidative Stress Using Deep Convolutional Neural Network

Awais Khan Nawabi | Sheng Jinfang | ... | Baidenger Agyekum Twumasi
  • Special Issue
  • - Volume 2022
  • - Article ID 2657713
  • - Research Article

(−)-Epicatechin Reduces Neuroinflammation, Protects Mitochondria Function, and Prevents Cognitive Impairment in Sepsis-Associated Encephalopathy

Jianmin Ling | Yanqing Wu | ... | Minghao Fang
  • Special Issue
  • - Volume 2022
  • - Article ID 4759963
  • - Review Article

Mechanisms of Mitochondrial Malfunction in Alzheimer’s Disease: New Therapeutic Hope

Showkat Ul Nabi | Andleeb Khan | ... | Bairong Shen
  • Special Issue
  • - Volume 2022
  • - Article ID 9253916
  • - Research Article

Hippocampal Mitochondrial Abnormalities Induced the Dendritic Complexity Reduction and Cognitive Decline in a Rat Model of Spinal Cord Injury

Xvlei Hu | Liang Wu | ... | Hechun Xia
  • Special Issue
  • - Volume 2022
  • - Article ID 8482149
  • - Review Article

The Molecular Mechanism of Retina Light Injury Focusing on Damage from Short Wavelength Light

Bin Fan | ChunXia Zhang | ... | Guang-Yu Li
  • Special Issue
  • - Volume 2022
  • - Article ID 7511393
  • - Research Article

Dexmedetomidine Can Enhance PINK1/Parkin-Mediated Mitophagy in MPTP-Induced PD Mice Model by Activating AMPK

Cheng Chen | Yaohua Chen | ... | Oumei Cheng
  • Special Issue
  • - Volume 2022
  • - Article ID 9565545
  • - Research Article

Molecular Signatures of Mitochondrial Complexes Involved in Alzheimer’s Disease via Oxidative Phosphorylation and Retrograde Endocannabinoid Signaling Pathways

Fenqin Chen | Jun Bai | ... | Zhike Zhou
  • Special Issue
  • - Volume 2022
  • - Article ID 1764589
  • - Research Article

Neuroprotective Effect of HIIT against GFAP Hypertrophy through Mitochondrial Dynamics in APP/PS1 Mice

Qianqian Liu | Xiaonan Fu | ... | Jianshe Wei
  • Special Issue
  • - Volume 2022
  • - Article ID 4906434
  • - Review Article

Mitophagy in Traumatic Brain Injury: A New Target for Therapeutic Intervention

Mingrui Zhu | Xinqi Huang | ... | Mingyang Zhang
Oxidative Medicine and Cellular Longevity
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