Redox Signaling in Brain Aging and Neurodegeneration
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: 28 September 2025 | Viewed by 826
Special Issue Editor
Interests: neurodegenerative disease; mitochondrial dysfunction; oxidative stress; Parkinson’s diseases; molecular mechanisms
Special Issues, Collections and Topics in MDPI journals
Special Issue Information
Dear Colleagues,
Redox signaling is increasingly recognized as a critical factor in brain aging and neurodegenerative diseases. While physiological levels of reactive oxygen and nitrogen species serve as essential signaling molecules, their dysregulation contributes to oxidative stress, mitochondrial dysfunction, proteostasis defects, and neuroinflammation, ultimately leading to neuronal damage. Brain aging is characterized by a gradual decline in antioxidant defenses, rendering neural tissues more susceptible to redox imbalances. This vulnerability is further exacerbated in neurodegenerative diseases such as Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, and amyotrophic lateral sclerosis, where disrupted redox signaling intersects with proteostasis alteration, inflammation, and synaptic dysfunction.
This Special Issue explores the intricate mechanisms underlying redox signaling in brain aging and its transition to neurodegenerative states. Key topics include the role of redox-sensitive signaling pathways, the impact of oxidative damage on neuronal networks, and the therapeutic potential of targeting redox imbalance. By integrating insights from molecular biology, neuroscience, and translational research, this issue aims to advance our understanding of redox dynamics in brain health and disease, ultimately paving the way for innovative approaches to mitigate neurodegeneration and promote healthy aging.
Dr. Marco Bisaglia
Guest Editor
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Keywords
- aging
- autophagy
- brain
- Alzheimer disease
- amyotrophic lateral sclerosis
- Friedreich ataxia
- Huntington disease
- neurodegeneration
- oxidative stress
- protein aggregation
- Parkinson’s disease
- reactive oxygen species
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