ReviewCell & bioscience2024
Cellular and molecular mechanisms of aspartoacylase and its role in Canavan disease.
Review in Cell & bioscience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 10 citations in OpenAlex.
- From neuronal marker to metabolic mediator: Expanding the functional landscape of N-acetylaspartate in the central nervous system and the periphery.Neural regeneration research · 2026Article
- The Emerging Role of N-Acetylaspartate in Cancer.International journal of molecular sciences · 2026Review
- Single cell analysis of developing Merkel cells reveals the emergence of non-coding RNA biotypes as a hallmark of terminal differentiation.Cell death and differentiation · 2026Article
- Fibroblastic aspartoacylase suppresses TGFβ-mediated responses and cancer progression.Nature communications · 2026Article
- Loss of Kv8.2 in the Mouse Retina Is Associated With Altered One-Carbon Metabolism.Journal of neurochemistry · 2026Article
- Human iPSC-derived neural progenitor cells rescue motor function and brain pathology in symptomatic Canavan disease mice.Stem cell reports · 2026Article
- Enhancing Spatial Transcriptomics via Spatially Constrained Matrix Decomposition with EDGES.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Short-chain PFAS exposure during gestation and breastfeeding alters learning and memory in adulthood: possible mechanisms related to brain development.Frontiers in toxicology · 2025Article
- Impact of Histone Acetyltransferases and Histone Deacetylases on Adult Brain Myelin Plasticity.Results and problems in cell differentiation · 2025Review
- UrineHuman gene therapy · 2024Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Canavan disease is an autosomal recessive and lethal neurological disorder, characterized by the spongy degeneration of the white matter in the brain. The disease is caused by a deficiency of the cytosolic aspartoacylase (ASPA) enzyme, which catalyzes the hydrolysis of N-acetyl-aspartate (NAA), an abundant brain metabolite, into aspartate and acetate. On the physiological level, the mechanism of pathogenicity remains somewhat obscure, with multiple, not mutually exclusive, suggested hypotheses. At the molecular level, recent studies have shown that most disease linked ASPA gene variants lead to a structural destabilization and subsequent proteasomal degradation of the ASPA protein variants, and accordingly Canavan disease should in general be considered a protein misfolding disorder. Here, we comprehensively summarize the molecular and cell biology of ASPA, with a particular focus on disease-linked gene variants and the pathophysiology of Canavan disease. We highlight the importance of high-throughput technologies and computational prediction tools for making genotype-phenotype predictions as we await the results of ongoing trials with gene therapy for Canavan disease.
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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.