ArticleMetabolic brain disease2016
Impaired PLP-dependent metabolism in brain samples from Huntington disease patients and transgenic R6/1 mice.
Article in Metabolic brain disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 12 citations in OpenAlex.
- Vitamin B6 produced by gut microbiome regulates host behavioral phenotypes through dopaminergic metabolism.Gut microbes · 2026Article
- Oxidative Stress in Huntington's Disease.Biomolecules · 2025Review
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- Vitamin B3 Biotech · 2023Article
- The impact ofAging · 2022Article
- Neuroprotective Roles of the Reverse Transsulfuration Pathway in Alzheimer's Disease.Frontiers in aging neuroscience · 2021Article
- Metabolic profiling of presymptomatic Huntington's disease sheep reveals novel biomarkers.Scientific reports · 2017Article
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Authors and funding
8 authors at 5 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Oxidative stress has been described as important to Huntington disease (HD) progression. In a previous HD study, we identified several carbonylated proteins, including pyridoxal kinase and antiquitin, both of which are involved in the metabolism of pyridoxal 5´-phosphate (PLP), the active form of vitamin B6. In the present study, pyridoxal kinase levels were quantified and showed to be decreased both in HD patients and a R6/1 mouse model, compared to control samples. A metabolomic analysis was used to analyze metabolites in brain samples of HD patients and R6/1 mice, compared to control samples using mass spectrometry. This technique allowed detection of increased concentrations of pyridoxal, the substrate of pyridoxal kinase. In addition, PLP, the product of the reaction, was decreased in striatum from R6/1 mice. Furthermore, glutamate and cystathionine, both substrates of PLP-dependent enzymes were increased in HD. This reinforces the hypothesis that PLP synthesis is impaired, and could explain some alterations observed in the disease. Together, these results identify PLP as a potential therapeutic agent.
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