ArticleJournal of inherited metabolic disease2001
IGF-1 and bFGF reduce glutaric acid and 3-hydroxyglutaric acid toxicity in striatal cultures.
Article in Journal of inherited metabolic disease, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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Who cites it
16 citing papers in PubMed, 42 citations in OpenAlex.
- Screening method and metabolic analysis of plant anti-aging microorganisms via ammonia-induced senescence in the duckweedFrontiers in plant science · 2024Article
- Glutaric acid-mediated apoptosis in primary striatal neurons.BioMed research international · 2014Article
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- Huntington's Disease: From Mutant Huntingtin Protein to Neurotrophic Factor Therapy.International journal of biomedical science : IJBS · 2011Article
- Potential drugs and methods for preventing or delaying the progression of Huntington's disease.Recent patents on CNS drug discovery · 2011Article
- Small molecule BDNF mimetics activate TrkB signaling and prevent neuronal degeneration in rodents.The Journal of clinical investigation · 2010Article
- Article
- Energy metabolism is compromised in skeletal muscle of rats chronically-treated with glutaric acid.Metabolic brain disease · 2007Article
- Infant mice with glutaric acidaemia type I have increased vulnerability to 3-nitropropionic acid toxicity.Journal of inherited metabolic disease · 2006Article
- Huntington's disease and neurogenesis: FGF-2 to the rescue?Proceedings of the National Academy of Sciences of the United States of America · 2005Article
- FGF-2 promotes neurogenesis and neuroprotection and prolongs survival in a transgenic mouse model of Huntington's disease.Proceedings of the National Academy of Sciences of the United States of America · 2005Article
- Glutaric acid administration impairs energy metabolism in midbrain and skeletal muscle of young rats.Neurochemical research · 2005Article
- Promotion of oxidative stress by 3-hydroxyglutaric acid in rat striatum.Journal of inherited metabolic disease · 2005Article
- Modulation of glutamatergic and GABAergic neurotransmission in glutaryl-CoA dehydrogenase deficiency.Journal of inherited metabolic disease · 2004Review
- Vascular dysfunction as an additional pathomechanism in glutaric aciduria type I.Journal of inherited metabolic disease · 2004Review
- Excitotoxicity and bioenergetics in glutaryl-CoA dehydrogenase deficiency.Journal of inherited metabolic disease · 2004Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Glutaric acid (GA) and 3-hydroxyglutaric acid (3GA) are thought to contribute to the degeneration of the caudate and putamen that is seen in some children with glutaric acidaemia type I, a metabolic disorder caused by a glutaryl-CoA dehydrogenase deficiency. This study assessed the neurotoxicity of GA and 3GA (0-50 mmol/L) compared to quinolinic acid (QUIN) in striatal and cortical cultures. All three acids were neurotoxic in a dose-dependent manner; however, GA and 3GA were both more toxic than QUIN. The neurotoxic effects of low concentrations of GA or 3GA were additive to QUIN toxicity. A series of hormones and growth factors were tested for protection against GA and 3GA toxicity. Insulin (5-500 microU /ml), basic fibroblast growth factor (bFGF; 10 ng/ml), insulin-like growth factor (IGF-1; 50 ng/ml), brain-derived neurotrophic factor (BDNF; 10 ng/ml), glial-derived neurotrophic factor (GDNF; 10 ng/ml), and two glutamate antagonists were evaluated in brain cultures to which 7 mmol/L GA or 3GA were added. GA and 3GA neurotoxicities were prevented by bFGF. Attenuation of 3GA-induced neurotoxicity was seen with insulin (5 microU/ml) and IGF-1. BDNF and GDNF had no effects on neuronal survival. Glutamate antagonists MK801 (10 micromol/L) and NBQX (10 micromol/L) failed to prevent GA or 3GA neurotoxicity. We conclude that GA and 3GA are neurotoxic in cultures of embryonic rat striatum and cortex. Striatal neurons were rescued from death by bFGF and IGF-1 but not by glutamate antagonist, suggesting that toxicity in this embryonic system is not necessarily mediated by glutamate receptors.
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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.