Review of redox molecules NAD, NADPH and GSH in aging and neurodegeneration
This review examines how falling levels of NAD, NADPH and GSH and an imbalance between their oxidized and reduced forms relate to aging and neurodegenerative disorders, and discusses experimental strategies to regulate these compounds. [1]
Automatic summary · not editorially reviewed
The key findings
The review states that oxidative stress plays a key role in the development of aging and neurodegenerative disorders such as Alzheimer's, Parkinson's, Huntington's disease and multiple sclerosis. [1]
Under pathological conditions, NAD, NADPH and GSH concentrations decrease and an imbalance between their oxidized and reduced forms develops. [1]
The authors suggest that insights into redox homeostasis may contribute to interventions with the potential of increasing the human lifespan. [1]
The source at a glance
- Study type / format
- Review (abstract only)
- Population / context
- People with aging and neurodegenerative disorders such as Alzheimer's, Parkinson's, Huntington's disease and multiple sclerosis, as discussed in a review
- Summary based on
- Study abstract
- Original publication
- July 23, 2026
Redox imbalance in aging and neurodegeneration
The review states that oxidative stress plays a key role in the development of aging and several neurodegenerative disorders, including Alzheimer's disease, Parkinson's disease, Huntington's disease and multiple sclerosis. Coupled molecules in reduction-oxidation (redox) reactions regulate central signaling pathways and ensure that protective cell mechanisms are activated when needed. These redox couples include the oxidized and reduced forms of nicotinamide adenine dinucleotide (NAD/NADH), nicotinamide adenine dinucleotide phosphate (NADP/NADPH) and glutathione (GSSG/GSH).
Supporting source [1]
Lower NAD, NADPH and GSH under pathological conditions
According to the review, concentrations of NAD, NADPH and GSH decrease under pathological conditions, and an imbalance develops between the oxidized and reduced forms of these molecules. The review focuses on the mechanisms behind these changes and their possible consequences for neurodegenerative processes and aging. It also evaluates experimental studies on metabolic and genetic abnormalities linked to altered NAD, NADPH and GSH concentrations.
Supporting source [1]
Mitochondria, neuroprotection and lifespan hopes
The review highlights current research on strategies to regulate these compounds for neuroprotective purposes. Special attention goes to the interconnection between disturbed redox homeostasis and mitochondrial dysfunction, which the review describes as increasingly recognized as a crucial step in neurodegeneration. The authors suggest that these insights may contribute to innovative interventions targeting redox homeostasis, with the potential of increasing the human lifespan.
Supporting source [1]
How to interpret this
This is an abstract of a review; the full text was not reviewed. The abstract reports no study design, sample, follow-up or outcome data of its own. The lifespan remark is a stated potential, not a demonstrated human benefit, and the described links between redox imbalance and disease are associations, not proven causes.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Iskusnykh IY, Kryl'skii ED, Popova TN, Zakharova AA. · europepmc.org · July 23, 2026