ArticleMolecular neurobiology2013
Acute and chronic administration of the branched-chain amino acids decreases nerve growth factor in rat hippocampus.
Article in Molecular neurobiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.
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Who cites it
20 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.
- The use of BCAA to decrease delayed-onset muscle soreness after a single bout of exercise: a systematic review and meta-analysis.Amino acids · 2021Pooled it
- Effects of branched-chain amino acids on glucose metabolism in obese, prediabetic men and women: a randomized, crossover study.The American journal of clinical nutrition · 2019Trial
- Neuronal Metabolism of Branched-Chain Amino Acids Alleviates Lifespan Reduction Caused by High-Salt Diet in Drosophila.Journal of molecular neuroscience : MN · 2026Article
- Review
- CSF amino acid profiles in ICV-streptozotocin-induced sporadic Alzheimer's disease in male Wistar rat: a metabolomics and systems biology perspective.FEBS open bio · 2024Article
- Coadministration of tianeptine alters behavioral parameters and levels of neurotrophins in a chronic model of Maple Syrup Urine disease.Metabolic brain disease · 2022Article
- Is the Brain Undernourished in Alzheimer's Disease?Nutrients · 2022Article
- Administration of branched-chain amino acids alters epigenetic regulatory enzymes in an animal model of Maple Syrup Urine Disease.Metabolic brain disease · 2021Article
- Hippocampal metabolism of amino acids by L-amino acid oxidase is involved in fear learning and memory.Scientific reports · 2018Article
- Evaluation of plasma biomarkers of inflammation in patients with maple syrup urine disease.Journal of inherited metabolic disease · 2018Article
- Branched-chain amino acids and Alzheimer's disease: a Mendelian randomization analysis.Scientific reports · 2017Article
- Acute and long-term effects of intracerebroventricular administration of α-ketoisocaproic acid on oxidative stress parameters and cognitive and noncognitive behaviors.Metabolic brain disease · 2017Article
- Serum Markers of Neurodegeneration in Maple Syrup Urine Disease.Molecular neurobiology · 2017Article
- Antioxidants reverse the changes in energy metabolism of rat brain after chronic administration of L.-tyrosine.Metabolic brain disease · 2017Article
- Amino Acid Catabolism in Alzheimer's Disease Brain: Friend or Foe?Oxidative medicine and cellular longevity · 2017Review
- Increased susceptibility to metabolic dysregulation in a mouse model of Alzheimer's disease is associated with impaired hypothalamic insulin signaling and elevated BCAA levels.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2016Article
- Intracerebroventricular administration of α-ketoisocaproic acid decreases brain-derived neurotrophic factor and nerve growth factor levels in brain of young rats.Metabolic brain disease · 2016Article
- Coadministration of branched-chain amino acids and lipopolysaccharide causes matrix metalloproteinase activation and blood-brain barrier breakdown.Molecular neurobiology · 2014Article
- Branched-chain amino acid metabolism: from rare Mendelian diseases to more common disorders.Human molecular genetics · 2014Review
- Behavioral responses in rats submitted to chronic administration of branched-chain amino acids.JIMD reports · 2014Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Maple syrup urine disease (MSUD) is a neurometabolic disorder caused by deficiency of the activity of the mitochondrial enzyme complex branched-chain α-keto acid dehydrogenase leading to accumulation of the branched-chain amino acids (BCAA) and their corresponding branched-chain α-keto acids. In this study, we examined the effects of acute and chronic administration of BCAA on protein levels and mRNA expression of nerve growth factor (NGF) considering that patients with MSUD present neurological dysfunction and cognitive impairment. Considering previous observations, it is suggested that oxidative stress may be involved in the pathophysiology of the neurological dysfunction of MSUD. We also investigated the influence of antioxidant treatment (N-acetylcysteine and deferoxamine) in order to verify the influence of oxidative stress in the modulation of NGF levels. Our results demonstrated decreased protein levels of NGF in the hippocampus after acute and chronic administration of BCAA. In addition, we showed a significant decrease in the expression of ngf in the hippocampus only following acute administration in 10-day-old rats. Interestingly, antioxidant treatment was able to prevent the decrease in NGF levels by increasing ngf expression. In conclusion, the results suggest that BCAA is involved in the regulation of NGF in the developing rat. Thus, it is possible that alteration of neurotrophin levels during brain maturation could be of pivotal importance in the impairment of cognition provoked by BCAA. Moreover, the decrease in NGF levels was prevented by antioxidant treatment, reinforcing that the hypothesis of oxidative stress can be an important pathophysiological mechanism underlying the brain damage observed in MSUD.
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