ArticleAnnals of neurology2015
Ablating N-acetylaspartate prevents leukodystrophy in a Canavan disease model.
Article in Annals of neurology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
31 citing papers in PubMed, 52 citations in OpenAlex.
- Discovery ofACS medicinal chemistry letters · 2026Article
- Cellular and molecular mechanisms of aspartoacylase and its role in Canavan disease.Cell & bioscience · 2024Review
- Astroglial conditional Slc13a3 knockout is therapeutic in murine Canavan leukodystrophy.Annals of clinical and translational neurology · 2024Article
- Developing a human iPSC-derived three-dimensional myelin spheroid platform for modeling myelin diseases.iScience · 2023Article
- SOX2 is essential for astrocyte maturation and its deletion leads to hyperactive behavior in mice.Cell reports · 2022Article
- 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
- AGC1 Deficiency: Pathology and Molecular and Cellular Mechanisms of the Disease.International journal of molecular sciences · 2022Review
- Dual-function AAV gene therapy reverses late-stage Canavan disease pathology in mice.Frontiers in molecular neuroscience · 2022Article
- Ablating the Transporter Sodium-Dependent Dicarboxylate Transporter 3 Prevents Leukodystrophy in Canavan Disease Mice.Annals of neurology · 2021Article
- High Throughput Screening Cascade To Identify Human AspartateACS chemical neuroscience · 2021Article
- Preclinical biodistribution, tropism, and efficacy of oligotropic AAV/Olig001 in a mouse model of congenital white matter disease.Molecular therapy. Methods & clinical development · 2021Article
- Canavan Disease as a Model for Gene Therapy-Mediated Myelin Repair.Frontiers in cellular neuroscience · 2021Review
- Emerging Concepts in Vector Development for Glial Gene Therapy: Implications for Leukodystrophies.Frontiers in cellular neuroscience · 2021Review
- Pathophysiology and Treatment of Canavan Disease.Neurochemical research · 2020Article
- Antisense Oligonucleotide Reverses Leukodystrophy in Canavan Disease Mice.Annals of neurology · 2020Article
- Neurological manifestations of organic acidurias.Nature reviews. Neurology · 2019Review
- Brain Nat8l Knockdown Suppresses Spongiform Leukodystrophy in an Aspartoacylase-Deficient Canavan Disease Mouse Model.Molecular therapy : the journal of the American Society of Gene Therapy · 2018Article
- Sox2 Is Essential for Oligodendroglial Proliferation and Differentiation during Postnatal Brain Myelination and CNS Remyelination.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Uncoupling N-acetylaspartate from brain pathology: implications for Canavan disease gene therapy.Acta neuropathologica · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Canavan disease is caused by inactivating ASPA (aspartoacylase) mutations that prevent cleavage of N-acetyl-L-aspartate (NAA), resulting in marked elevations in central nervous system (CNS) NAA and progressively worsening leukodystrophy. We now report that ablating NAA synthesis by constitutive genetic disruption of Nat8l (N-acetyltransferase-8 like) permits normal CNS myelination and prevents leukodystrophy in a murine Canavan disease model.
Indexed as
Identifiers
What OpenQuestion holds
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.