ArticleJournal of molecular neuroscience : MN
Expression of aspartoacylase activity in cultured rat macroglial cells is limited to oligodendrocytes.
Article in Journal of molecular neuroscience : MN. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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33 citing papers in PubMed, 100 citations in OpenAlex.
- Beyond Neurodegeneration: White Matter Vacuolation as a Primary Myelin Defect.International journal of molecular sciences · 2026Review
- Human iPSC-derived neural progenitor cells rescue motor function and brain pathology in symptomatic Canavan disease mice.Stem cell reports · 2026Article
- Cellular and molecular mechanisms of aspartoacylase and its role in Canavan disease.Cell & bioscience · 2024Review
- Metabolic partitioning in the brain and its hijacking by glioblastoma.Genes & development · 2023Review
- The pathogenesis of, and pharmacological treatment for, Canavan disease.Drug discovery today · 2022Review
- Increasing Aspartoacylase in the Central Amygdala: The Common Mechanism of Gastroprotective Effects of Monoamine-Based Antidepressants Against Stress.Frontiers in pharmacology · 2022Article
- Mapping the degradation pathway of a disease-linked aspartoacylase variant.PLoS genetics · 2021Article
- Neurometabolic abnormalities in the associative striatum in antipsychotic-naïve first episode psychosis patients.Psychiatry research. Neuroimaging · 2018Article
- Rescuing Canavan disease: engineering the wrong cell at the right time.Journal of inherited metabolic disease · 2017Article
- Clinically Distinct Phenotypes of Canavan Disease Correlate with Residual Aspartoacylase Enzyme Activity.Human mutation · 2017Article
- RedirectingJCI insight · 2017Article
- N-acetylaspartate supports the energetic demands of developmental myelination via oligodendroglial aspartoacylase.Neurobiology of disease · 2016Article
- Astroglial redistribution of aquaporin 4 during spongy degeneration in a Canavan disease mouse model.Journal of molecular neuroscience : MN · 2014Article
- Rat strain differences in brain structure and neurochemistry in response to binge alcohol.Psychopharmacology · 2014Article
- N-Acetylaspartate reductions in brain injury: impact on post-injury neuroenergetics, lipid synthesis, and protein acetylation.Frontiers in neuroenergetics · 2013Review
- A mechanism of rapidly reversible cerebral ventricular enlargement independent of tissue atrophy.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2013Article
- Long-term follow-up after gene therapy for canavan disease.Science translational medicine · 2012Article
- Expression and localization of myosin-1d in the developing nervous system.Brain research · 2012Article
- Article
- Regulation of oligodendrocyte development and myelination by glucose and lactate.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
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Authors and funding
4 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
N-acetyl-L-aspartate (NAA) is an important osmolyte in the vertebrate brain and eye, and its cyclical metabolism is accomplished in two separate compartments. In the brain, NAA is synthesized primarily in neurons, and after its regulated release, NAA is hydrolyzed by aspartoacylase, which is present in a glial-associated compartment. However, the precise nature of this hydrolytic compartment has remained obscure. It has been proposed that one role of aspartoacylase in the central nervous system (CNS) is as part of a molecular water pump (MWP) that uses the NAA intercompartmental cycle to remove nerve cell metabolic water against a water gradient and that oligodendrocytes comprise the second compartment in this metabolic sequence. The absence of aspartoacylase activity in Canavan disease (CD), a rare early onset genetic spongiform leukodystrophy, is associated with CNS edema, intramyelinic swelling and a progressive loss of oligdendrocytes. In order to evaluate the MWP hypothesis and its possible relationship to the etiology of CD further, both oligodendrocytes and astrocytes obtained from neonatal rat brain were grown in culture and tested for the presence of aspartoacylase activity. The results of this study show for the first time that aspartoacylase activity is expressed only in oligodendrocytes. The meaning of this observation in understanding the function of the NAA metabolic cycle is discussed.
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