Oxidative Stress Mechanisms and Parkinson's Disease Treatment
A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".
Deadline for manuscript submissions: 31 May 2025 | Viewed by 866
Special Issue Editor
Special Issue Information
Dear Colleagues,
It has been 57 years since the introduction of L-dopa in the treatment of idiopathic Parkinson's disease, and it is still the most effective drug in the treatment of this disease despite severe side effects after chronic treatment for 4 to 6 years. However, the failure of clinical studies involving antioxidants such as coenzyme Q raises the need for a thorough analysis of the role of oxidative stress in triggering the loss of neuromelanin-containing dopaminergic neurons of the nigrostriatal system, as well as possible factors that have influenced the failure of these clinical studies. In addition to the role of oxidative stress in the loss of dopaminergic neurons containing neuromelanin from the nigrostriatal system, other mechanisms are also involved, such as the formation of neurotoxic oligomers of alpha-synuclein, mitochondrial dysfunction, endoplasmic reticulum stress, dysfunction of both lysosomal and proteasomal protein degradation systems, and neuroinflammation. Therefore, in order to develop new treatments for idiopathic Parkinson's disease, a critical discussion of both the mechanisms that trigger the loss of neuromelanin-containing dopaminergic neurons from the nigrostriatal system and the preclinical models that we use to evaluate the effectiveness of a drug in this disease is required.
I invite you to submit your latest research findings, hypothesis papers, and review articles to this Special Issue, which will help us both to understand the failure of these clinical studies and to shed light on how to search for new drugs that can halt or modify the progression of this disease.
Prof. Dr. Juan Segura-Aguilar
Guest Editor
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Keywords
- Parkinson’s disease
- dopamine
- dopamine oxidation
- neuromelanin
- dopaminergic neurons
- antioxidants
- neuroprotection
- neurodegeneration
- oxidative stress
- protein degradation dysfunction
- neuroinflammation
- mitochondrial dysfunction
- endoplasmic reticulum stress
- alpha-synuclein oligomers
- glutathione
- glutathione transferase
- DT-diaphorase
- preclinical model for Parkinson's disease
- VMAT2
- dopamine transporter
- tyrosine hydroxylase
- dopamine-derived orto-quinones
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