ArticleJournal of neurochemistry2008
Elevated oxidative stress and sensorimotor deficits but normal cognition in mice that cannot synthesize ascorbic acid.
Article in Journal of neurochemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
56 citing papers in PubMed, 1 synthesis or guideline pooled it, 98 citations in OpenAlex.
- The Effect of Perioperative Vitamin C on Postoperative Analgesic Consumption: A Meta-Analysis of Randomized Controlled Trials.Nutrients · 2020Pooled it
- Noninvasive quantification of human brain antioxidant concentrations after an intravenous bolus of vitamin C.NMR in biomedicine · 2011Trial
- Acupuncture: A Promising Non-Pharmacological Approach to Parkinson's Disease Management.Brain and behavior · 2026Review
- Vitamin C Transport Deficiency Alters Striatal Dopamine Gene Expression and Metabolism in YAC128 Huntington Disease Mice.Genes, brain, and behavior · 2025Article
- Modulation of microglia activation by the ascorbic acid transporter SVCT2.Brain, behavior, and immunity · 2024Article
- Sex and organ specific proteomic responses to vitamin C deficiency in the brain, heart, liver, and spleen of Gulo-/- mice.PloS one · 2024Article
- Electroacupuncture at ST25 corrected gut microbial dysbiosis and SNpc lipid peroxidation in Parkinson's disease rats.Frontiers in microbiology · 2024Article
- Druggable transcriptomic pathways revealed in Parkinson's patient-derived midbrain neurons.NPJ Parkinson's disease · 2022Article
- Ascorbate Is a Primary Antioxidant in Mammals.Molecules (Basel, Switzerland) · 2022Review
- Identification of an exporter that regulates vitamin C supply from blood to the brain.iScience · 2022Article
- Review
- Ascorbate deficiency decreases dopamine release in guloJournal of neurochemistry · 2021Article
- Article
- Decreased content of ascorbic acid (vitamin C) in the brain of knockout mouse models of Na+,K+-ATPase-related neurologic disorders.PloS one · 2021Article
- A Cecal Slurry Mouse Model of Sepsis Leads to Acute Consumption of Vitamin C in the Brain.Nutrients · 2020Article
- Lentiviral-mediated knock-down of GD3 synthase protects against MPTP-induced motor deficits and neurodegeneration.Neuroscience letters · 2019Article
- Altered glutamate clearance in ascorbate deficient mice increases seizure susceptibility and contributes to cognitive impairment in APP/PSEN1 mice.Neurobiology of aging · 2018Article
- Antioxidants prevent inflammation and preserve the optic projection and visual function in experimental neurotrauma.Cell death & disease · 2018Article
- Oxidative Stress Levels in the Brain Are Determined by Post-Mortem Interval and Ante-Mortem Vitamin C State but Not Alzheimer's Disease Status.Nutrients · 2018Article
- Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Oxidative stress is implicated in the cognitive deterioration associated with normal aging as well as neurodegenerative disorders such as Alzheimer's and Parkinson's diseases. We investigated the effect of ascorbic acid (vitamin C) on oxidative stress, cognition, and motor abilities in mice null for gulono-gamma-lactone oxidase (Gulo). Gulo-/- mice are unable to synthesize ascorbic acid and depend on dietary ascorbic acid for survival. Gulo-/- mice were given supplements that provided them either with ascorbic acid levels equal to- or slightly higher than wild-type mice (Gulo-sufficient), or lower than physiological levels (Gulo-low) that were just enough to prevent scurvy. Ascorbic acid is a major anti-oxidant in mice and any reduction in ascorbic acid level is therefore likely to result in increased oxidative stress. Ascorbic acid levels in the brain and liver were higher in Gulo-sufficient mice than in Gulo-low mice. F(4)-neuroprostanes were elevated in cortex and cerebellum in Gulo-low mice and in the cortex of Gulo-sufficient mice. All Gulo-/- mice were cognitively normal but had a strength and agility deficit that was worse in Gulo-low mice. This suggests that low levels of ascorbic acid and elevated oxidative stress as measured by F(4)-neuroprostanes alone are insufficient to impair memory in the knockouts but may be responsible for the exacerbated motor deficits in Gulo-low mice, and ascorbic acid may have a vital role in maintaining motor abilities.
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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.