ArticleACS chemical neuroscience2013
Brain glucose-6-phosphate dehydrogenase protects against endogenous oxidative DNA damage and neurodegeneration in aged mice.
Article in ACS chemical neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
What it found
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Who cites it
34 citing papers in PubMed, 62 citations in OpenAlex.
- The Role of Cytochrome P450 Holoenzyme Metabolism in the Origin of Neuropathologies.International journal of molecular sciences · 2026Review
- Redox Molecules in Aging and Neurodegenerative Disorders.International journal of molecular sciences · 2026Review
- Neuronal loss of the pentose phosphate pathway in the living nervous system is causally linked to [NADPH] reduction and elevated oxidative stress.The Journal of physiology · 2026Article
- G6PD deficiency in brain induces schizophrenia-like behaviors and synaptic dysfunction.Translational psychiatry · 2025Article
- Redox System Dysfunction as a Key Mechanism in Autism Spectrum Disorder Pathogenesis.International journal of molecular sciences · 2025Review
- Neural Metabolic Networks: Key Elements of Healthy Brain Function.Journal of neurochemistry · 2025Review
- Enhancing NADPH to restore redox homeostasis and lysosomal function in G6PD-deficient microglia.Heliyon · 2025Article
- Dynamics of Redox Metabolism during Complete Metamorphosis of Insects: Insights from the Sunflower CaterpillarAntioxidants (Basel, Switzerland) · 2024Article
- Article
- Age-regulated cycling metabolites are relevant for behavior.Aging cell · 2024Article
- Homeostasis of carbohydrates and reactive oxygen species is critically changed in the brain of middle-aged mice: Molecular mechanisms and functional reasons.BBA advances · 2023Article
- Platinum-resistance in epithelial ovarian cancer: an interplay of epithelial-mesenchymal transition interlinked with reprogrammed metabolism.Journal of translational medicine · 2022Article
- Review
- Boosting the Discovery of Small Molecule Inhibitors of Glucose-6-Phosphate Dehydrogenase for the Treatment of Cancer, Infectious Diseases, and Inflammation.Journal of medicinal chemistry · 2022Review
- Metabolic Features of Brain Function with Relevance to Clinical Features of Alzheimer and Parkinson Diseases.Molecules (Basel, Switzerland) · 2022Review
- Glial Cell Line-Derived Neurotrophic Factor and Focal Ischemic Stroke.Neurochemical research · 2021Review
- Treatment strategies for glucose-6-phosphate dehydrogenase deficiency: past and future perspectives.Trends in pharmacological sciences · 2021Review
- Middle aged turn point in parameters of oxidative stress and glucose catabolism in mouse cerebellum during lifespan: minor effects of every-other-day fasting.Biogerontology · 2021Article
- GLAST-CreERGlia · 2020Article
- A Dual Role of ATM in Ischemic Preconditioning and Ischemic Injury.Cellular and molecular neurobiology · 2020Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Glucose-6-phosphate dehydrogenase (G6PD) protects the embryo from endogenous and xenobiotic-enhanced oxidative DNA damage and embryopathies. Here we show in aged mice that G6PD similarly protects against endogenous reactive oxygen species (ROS)-mediated neurodegeneration. In G6PD-normal (G6PD(+/+)) and heterozygous (G6PD(+/def)) and homozygous (G6PD(def/def)) G6PD-deficient male and female mice at about 2 years of age, oxidative DNA damage in various brain regions was assessed by 8-oxo-2'-deoxyguanosine formation using high-performance liquid chromatography and immunohistochemistry. Morphological changes in brain sections were assessed by H&E staining. DNA oxidation was increased in G6PD(def/def) mice in the cortex (p < 0.02), hippocampus (p < 0.01) and cerebellum (p < 0.006) compared to G6PD(+/+) mice, and was localized to distinct cell types. Histologically, in G6PD(+/def) mice, enhanced regionally and cellularly specific neurodegenerative changes were observed in those brain regions exhibiting elevated DNA oxidation, with a 53% reduction in the Purkinje cell count. These results show G6PD is important in protecting against the neurodegenerative effects of endogenous ROS in aging, and suggest that common hereditary G6PD deficiencies may constitute a risk factor for some neurodegenerative diseases.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.