ReviewJournal of molecular neuroscience : MN2003
Brain N-acetylaspartate as a molecular water pump and its role in the etiology of Canavan disease: a mechanistic explanation.
Review in Journal of molecular neuroscience : MN, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
28 citing papers in PubMed, 1 synthesis or guideline pooled it, 102 citations in OpenAlex.
- Meta-analytic evidence of elevated choline, reduced N-acetylaspartate, and normal creatine in schizophrenia and their moderation by measurement quality, echo time, and medication status.NeuroImage. Clinical · 2023Pooled it
- Glyceryl triacetate for Canavan disease: a low-dose trial in infants and evaluation of a higher dose for toxicity in the tremor rat model.Journal of inherited metabolic disease · 2009Trial
- Diagnostic value of quantitative MR spectroscopy metabolite ratios for Canavan disease.Frontiers in radiology · 2026Article
- Deep Intronic SVA_E Retrotransposition as a Novel Factor in Canavan Disease Pathogenesis.Human gene therapy · 2025Article
- Cellular and molecular mechanisms of aspartoacylase and its role in Canavan disease.Cell & bioscience · 2024Review
- White matter and neurochemical mechanisms underlying age-related differences in motor processing speed.iScience · 2023Article
- The pathogenesis of, and pharmacological treatment for, Canavan disease.Drug discovery today · 2022Review
- High Throughput Screening Cascade To Identify Human AspartateACS chemical neuroscience · 2021Article
- Mapping the degradation pathway of a disease-linked aspartoacylase variant.PLoS genetics · 2021Article
- Brain Metabolite, N-Acetylaspartate Is a Potent Protein Aggregation Inhibitor.Frontiers in cellular neuroscience · 2021Article
- N-Acetylaspartate Is an Important Brain Osmolyte.Biomolecules · 2020Article
- The Neurobiology of Depression: an Integrated Overview from Biological Theories to Clinical Evidence.Molecular neurobiology · 2017Review
- Oligodendrocytes Do Not Export NAA-Derived Aspartate In Vitro.Neurochemical research · 2017Article
- N-acetylaspartate supports the energetic demands of developmental myelination via oligodendroglial aspartoacylase.Neurobiology of disease · 2016Article
- Inherited and acquired disorders of myelin: The underlying myelin pathology.Experimental neurology · 2016Review
- A combined diffusion tensor imaging and magnetic resonance spectroscopy study of patients with schizophrenia.Schizophrenia research · 2016Article
- A new mouse model of Canavan leukodystrophy displays hearing impairment due to central nervous system dysmyelination.Disease models & mechanisms · 2014Article
- Astroglial redistribution of aquaporin 4 during spongy degeneration in a Canavan disease mouse model.Journal of molecular neuroscience : MN · 2014Article
- Brain proton magnetic resonance spectroscopy of alcohol use disorders.Handbook of clinical neurology · 2014Review
- N-acetyl peak in proton MR spectroscopy of metastatic mucinous adenocarcinoma of brain.Clinical neuroradiology · 2013Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
N-acetyl-L-aspartate (NAA), an abundant amino acid present in the vertebrate brain, is synthesized and stored primarily in neurons. Its metabolism is also dynamic, with NAA turning over more than once each day by its regulated efflux into extracellular fluid (ECF), cycling between an anabolic L-aspartate acetylating compartment in neurons and a catabolic NAA deacetylating compartment in oligodendrocytes. An inborn error in NAA metabolism results in Canavan disease (CD), a rare and usually fatal early-onset autosomal recessive human central nervous system (CNS) disease, caused by failure of the catabolic metabolism of NAA resulting from a lack of sufficient amidohydrolase II activity in oligodendrocytes. Various hypotheses regarding the metabolism of NAA and its role have been considered, and although NAA may perform several functions in the CNS, an important role of NAA appears to be osmoregulatory. Based on this role, an osmotic-hydrostatic mechanism for the etiology of the CD phenotype is proposed. In CD, the daily addition of 13375 Pascals (0.132 atmospheres or 1.94 lbs per square inch) of hydrostatic pressure to brain ECF, on the brain cell side of brain-barrier epithelial membranes, resulting from the continuous synthesis and efflux of NAA, is considered to be responsible for the syndrome.
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Registered trials
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.