ReviewDrug design, development and therapy2013
Developing therapeutic approaches for metachromatic leukodystrophy.
Review in Drug design, development and therapy, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02559830 (A Phase I/II Clinical Trial of Lentiviral Hematopoietic Stem Cell Gene Therapy for Treatment of Developed Metachromatic Leukodystrophy and Adrenoleukodystrophy), which is not on this map. Cited by 35 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.
A Phase I/II Clinical Trial of Lentiviral Hematopoietic Stem Cell Gene Therapy for Treatment of Developed Metachromatic Leukodystrophy and Adrenoleukodystrophy
Who cites it
35 citing papers in PubMed, 76 citations in OpenAlex.
- Juvenile metachromatic leukodystrophy caused by a rare genetic mutation.Neurogenetics · 2025Article
- Phytoconstituents of Withania somnifera (L.) Dunal (Ashwagandha) unveiled potential cerebroside sulfotransferase inhibitors: insight through virtual screening, molecular dynamics, toxicity, and reverse pharmacophore analysis.Journal of biological engineering · 2024Article
- Overview of Neuro-Ophthalmic Findings in Leukodystrophies.Journal of clinical medicine · 2024Article
- Biochemical and molecular analysis of pediatric patients with metachromatic leukodystrophy in South China: functional characterization of five novel ARSA variants.Metabolic brain disease · 2024Article
- Article
- Adeno-associated Virus-Mediated Gene Delivery Across the Blood-Brain Barrier.Advances in neurobiology · 2024Review
- Single Systemic Administration of a Gene Therapy Leading to Disease Treatment in Metachromatic LeukodystrophyThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Gene Therapy of Sphingolipid Metabolic Disorders.International journal of molecular sciences · 2023Review
- Understanding caregiver descriptions of initial signs and symptoms to improve diagnosis of metachromatic leukodystrophy.Orphanet journal of rare diseases · 2022Article
- Therapeutic advantages of combined gene/cell therapy strategies in a murine model of GM2 gangliosidosis.Molecular therapy. Methods & clinical development · 2022Article
- Case report: A compound heterozygous mutations inFrontiers in neurology · 2022Article
- Emerging cellular themes in leukodystrophies.Frontiers in cell and developmental biology · 2022Review
- Rare Diseases in Glycosphingolipid Metabolism.Advances in experimental medicine and biology · 2022Article
- Safety of Direct Intraparenchymal AAVrh.10-Mediated Central Nervous System Gene Therapy for Metachromatic Leukodystrophy.Human gene therapy · 2021Article
- Chinese Cases of Metachromatic Leukodystrophy with the Novel Missense Mutations in ARSA Gene.Journal of molecular neuroscience : MN · 2021Article
- Identification of a missense ARSA mutation in metachromatic leukodystrophy and its potential pathogenic mechanism.Molecular genetics & genomic medicine · 2020Article
- Brain Penetrable Inhibitors of Ceramide Galactosyltransferase for the Treatment of Lysosomal Storage Disorders.ACS medicinal chemistry letters · 2020Article
- Arylsulfatase A (ASA) in Parkinson's Disease: From Pathogenesis to Biomarker Potential.Brain sciences · 2020Review
- Lipophagy and Lipolysis Status in Lipid Storage and Lipid Metabolism Diseases.International journal of molecular sciences · 2020Review
- CNS-Targeting Therapies for Lysosomal Storage Diseases: Current Advances and Challenges.Frontiers in molecular biosciences · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Metachromatic leukodystrophy (MLD) is an autosomal recessive lysosomal disorder caused by the deficiency of arylsulfatase A (ASA), resulting in impaired degradation of sulfatide, an essential sphingolipid of myelin. The clinical manifestations of MLD are characterized by progressive demyelination and subsequent neurological symptoms resulting in severe debilitation. The availability of therapeutic options for treating MLD is limited but expanding with a number of early stage clinical trials already in progress. In the development of therapeutic approaches for MLD, scientists have been facing a number of challenges including blood-brain barrier (BBB) penetration, safety issues concerning therapies targeting the central nervous system, uncertainty regarding the ideal timing for intervention in the disease course, and the lack of more in-depth understanding of the molecular pathogenesis of MLD. Here, we discuss the current status of the different approaches to developing therapies for MLD. Hematopoietic stem cell transplantation has been used to treat MLD patients, utilizing both umbilical cord blood and bone marrow sources. Intrathecal enzyme replacement therapy and gene therapies, administered locally into the brain or by generating genetically modified hematopoietic stem cells, are emerging as novel strategies. In pre-clinical studies, different cell delivery systems including microencapsulated cells or selectively neural cells have shown encouraging results. Small molecules that are more likely to cross the BBB can be used as enzyme enhancers of diverse ASA mutants, either as pharmacological chaperones, or proteostasis regulators. Specific small molecules may also be used to reduce the biosynthesis of sulfatides, or target different affected downstream pathways secondary to the primary ASA deficiency. Given the progressive neurodegenerative aspects of MLD, also seen in other lysosomal diseases, current and future therapeutic strategies will be complementary, whether used in combination or separately at specific stages of the disease course, to produce better outcomes for patients afflicted with this devastating inherited disorder.
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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.