Special Issue

Topic: Mitochondrial Dysfunction in Neurodegenerative Diseases: Implications for Coenzyme Q10 Therapy

A Special Issue of Journal of Translational Genetics and Genomics

ISSN 2578-5281 (Online)

Submission deadline: 30 Nov 2024

Guest Editor(s)

Prof. Iain P. Hargreaves
School of Pharmacy and Biomolecular Sciences, Liverpool John Moores University, Liverpool, UK.

Special Issue Introduction

Mitochondrial dysfunction is implicated in various neurodegenerative disorders, such as Parkinson’s disease (PD), Alzheimer’s disease, and amyotrophic lateral sclerosis, as well as less common conditions like multisystem atrophy and progressive supranuclear palsy.  While the precise causes of mitochondrial dysfunction in many of these neurological disorders remain incompletely elucidated, it may result from oxidative stress-induced impairment of the mitochondrial respiratory chain (MRC) through various mechanisms. The brain, with its high metabolic demand and relatively low antioxidant defense systems, is particularly vulnerable to oxidative damage. Even slight redox imbalance can create an oxidative milieu, leading to tissue damage and activation of neuroinflammatory processes. However, in certain neurodegenerative disorders such as PD, mitochondrial dysfunction is not solely a secondary consequence of disease pathophysiology but may also be a key driver of early disease progression.  Given the important role of mitochondria in the maintenance and function of neuronal cells, impaired mitochondrial function  has been directly linked to neuronal morbidity due to a  number of factors, primarily progressive oxidative damage from increased reactive oxygen species (ROS) generation and diminished cellular energy generation. Therapeutic approaches targeting mitochondrial dysfunction in neurodegenerative disorders have therefore focused on the enhancement of MRC function and the amelioration of oxidative stress. Unfortunately, there remains a paucity of agents with therapeutic potential to enhance MRC function and bolster cellular antioxidant status, with coenzyme Q10 (CoQ10) and its synthetic analogs emerging as notable candidates.

The purpose of this special edition is to provide details about the pathophysiological mechanisms underlying mitochondrial dysfunction in neurodegenerative disorders and to outline the current therapeutic approaches involving CoQ10 and its analogs in the treatment of these disorders.

Submission Deadline

30 Nov 2024

Submission Information

For Author Instructions, please refer to https://www.oaepublish.com/jtgg/author_instructions
For Online Submission, please login at https://oaemesas.com/login?JournalId=jtgg&SpecialIssueId=jtgg240408
Submission Deadline: 30 Nov 2024
Contacts: Jixiang Zhao, Assistant Editor, jixiang.zhao@jtggjournal.com

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Journal of Translational Genetics and Genomics
ISSN 2578-5281 (Online)
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