ArticleJournal of inherited metabolic disease2010
Metabolic acetate therapy improves phenotype in the tremor rat model of Canavan disease.
Article in Journal of inherited metabolic disease, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 70 citations in OpenAlex.
- The Case for Vinegar Ingestion.Nutrients · 2026Review
- Gut Acetic Acid Alleviates Cognitive Impairment by Inhibiting Tau Hyperphosphorylation via Regulating FFAR3/Erk Pathway in Chronic Cerebral Ischemia Mice.Molecular neurobiology · 2025Article
- The Role of Short Chain Fatty Acids in Inflammation and Body Health.International journal of molecular sciences · 2024Review
- Cellular and molecular mechanisms of aspartoacylase and its role in Canavan disease.Cell & bioscience · 2024Review
- The pathogenesis of, and pharmacological treatment for, Canavan disease.Drug discovery today · 2022Review
- Therapeutic development for Canavan disease using patient iPSCs introduced with the wild-typeiScience · 2022Article
- Canavan Disease as a Model for Gene Therapy-Mediated Myelin Repair.Frontiers in cellular neuroscience · 2021Review
- Acetate Revisited: A Key Biomolecule at the Nexus of Metabolism, Epigenetics, and Oncogenesis - Part 2: Acetate and ACSS2 in Health and Disease.Frontiers in physiology · 2020Review
- Characteristics and advantages of adeno-associated virus vector-mediated gene therapy for neurodegenerative diseases.Neural regeneration research · 2019Review
- An MRI Study of the Metabolic and Structural Abnormalities in Obsessive-Compulsive Disorder.Frontiers in human neuroscience · 2019Article
- A translational perspective on histone acetylation modulators in psychiatric disorders.Psychopharmacology · 2018Review
- Behavioral impairment in SHATI/NAT8L knockout mice via dysfunction of myelination development.Scientific reports · 2017Article
- RedirectingJCI insight · 2017Article
- Increasing N-acetylaspartate in the Brain during Postnatal Myelination Does Not Cause the CNS Pathologies of Canavan Disease.Frontiers in molecular neuroscience · 2017Article
- Oral acetate supplementation attenuates N-methyl D-aspartate receptor hypofunction-induced behavioral phenotypes accompanied by restoration of acetyl-histone homeostasis.Psychopharmacology · 2016Article
- A combined diffusion tensor imaging and magnetic resonance spectroscopy study of patients with schizophrenia.Schizophrenia research · 2016Article
- N-Acetylaspartate Synthase Deficiency Corrects the Myelin Phenotype in a Canavan Disease Mouse Model But Does Not Affect Survival Time.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Acetate supplementation as a means of inducing glioblastoma stem-like cell growth arrest.Journal of cellular physiology · 2015Article
- Article
- Acetate supplementation modulates brain adenosine metabolizing enzymes and adenosine A₂A receptor levels in rats subjected to neuroinflammation.Journal of neuroinflammation · 2014Article
Corrections and comments
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Authors and funding
12 authors at 5 institutions in 3 countries.
Funding
Abstract
Genetic mutations that severely diminish the activity of aspartoacylase (ASPA) result in the fatal brain dysmyelinating disorder, Canavan disease. There is no effective treatment. ASPA produces free acetate from the concentrated brain metabolite, N-acetylaspartate (NAA). Because acetyl coenzyme A is a key building block for lipid synthesis, we postulated that the inability to catabolize NAA leads to a brain acetate deficiency during a critical period of CNS development, impairing myelination and possibly other aspects of brain development. We tested the hypothesis that acetate supplementation during postnatal myelination would ameliorate the severe phenotype associated with ASPA deficiency using the tremor rat model of Canavan disease. Glyceryltriacetate (GTA) was administered orally to tremor rats starting 7 days after birth, and was continued in food and water after weaning. Motor function, myelin lipids, and brain vacuolation were analyzed in GTA-treated and untreated tremor rats. Significant improvements were observed in motor performance and myelin galactocerebroside content in tremor rats treated with GTA. Further, brain vacuolation was modestly reduced, and these reductions were positively correlated with improved motor performance. We also examined the expression of the acetyl coenzyme A synthesizing enzyme acetyl coenzyme A synthase 1 and found upregulation of expression in tremor rats, with a return to near normal expression levels in GTA-treated tremor rats. These results confirm the critical role played by NAA-derived acetate in brain myelination and development, and demonstrate the potential usefulness of acetate therapy for the treatment of Canavan disease.
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