NAD+ Regulation in Antioxidant Defense and Neurodegenerative Diseases
A Special Issue of Antioxidants (ISSN 2076-3921) belonging to the section "Health Outcomes of Antioxidants and Oxidative Stress".
Deadline for manuscript submissions: 30 October 2026 | Viewed by 217
Editor
Interests: Nrf2; NAD+ supplements; enzyme mechanisms; hypoxia; oxidative stress; reporter assay; drug discovery
Special Issues, Collections and Topics in MDPI journals
Special Issue Information
Dear Colleagues,
The market of NAD (nicotinamide adenine dinucleotide) supplements in the form of liposomal NAD and NAD precursors (nicotinamide mononucleotide, nicotinamide riboside) is growing and approaching almost 1 billion USD a year. NAD levels significantly decline during aging and in various degenerative diseases, leading to mitochondrial dysfunction, impaired energy metabolism, and reduced cell survival. This depletion is a hallmark of neurodegenerative diseases (Alzheimer's, Parkinson's) and cardiovascular diseases, and this fact raises a question of whether NAD supplementation is a potential therapeutic strategy. A common view is that NAD+ supplementation largely improves mitochondrial energy production; however, very recent works show that the effect is more about activating the antioxidant defense rather than producing more ATP. In this respect, the new thematic issue of “Antioxidants” focuses on the research linking NAD supplementation to the possible improvements in general antioxidant status, activation of Nrf2-driven antioxidant program, and resistance towards ferroptosis in diseases with a significant contribution of oxidative stress. We welcome original research papers and reviews on preclinical and clinical studies or in vitro disease models of various diseases, as well as the identification of new protective mechanisms and pathways activated by NAD supplementation. The combined effects of NAD supplementation with Nrf2 activators are of special interest.
Prof. Dr. Irina G. Gazaryan
Guest Editor
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Keywords
- neurodegeneration
- dementia
- axonal degeneration
- stroke
- disease-modifying therapy
- antioxidant defense
- NAD assay
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