Evidence map›Paper›PMID 23966770›Full record

ReviewDrug design, development and therapy2013

Developing therapeutic approaches for metachromatic leukodystrophy.

Shilpa A Patil, Gustavo H B Maegawa

Registry-linked trialOpen access · goldAbstract readReview
In one paragraph

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.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.3field-weighted citation impact, top 7% of its field
1 · What the graph read from it

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.

2 · The registry

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.

NCT02559830 phase1 / phase2unknown statusnot on this mapstarted 2015, after this paper: background citation

A Phase I/II Clinical Trial of Lentiviral Hematopoietic Stem Cell Gene Therapy for Treatment of Developed Metachromatic Leukodystrophy and Adrenoleukodystrophy

TypeinterventionalSponsorShenzhen Second People's HospitalRan2015 to 2025Enrolled50ConditionsMetachromatic Leukodystrophy, AdrenoleukodystrophyArmstransduced CD34+ hematopoietic stem cell
3 · Its place in the literature

Who cites it

35 citing papers in PubMed, 76 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. 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 · 2023
    Article
  8. Gene Therapy of Sphingolipid Metabolic Disorders.International journal of molecular sciences · 2023
    Review
  9. Article
  10. Article
  11. Article
  12. Emerging cellular themes in leukodystrophies.Frontiers in cell and developmental biology · 2022
    Review
  13. Rare Diseases in Glycosphingolipid Metabolism.Advances in experimental medicine and biology · 2022
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Shilpa A PatilMcKusick-Nathans Institute of Genetic Medicine, The Johns Hopkins School of Medicine, Baltimore, MD, USA.
Gustavo H B Maegawa
Johns Hopkins University · US

Funding

Development of a HTS Assay for a Neurological Lysosomal DiseaseR01NS079655 · NINDS · UNIVERSITY OF FLORIDA · PI MAEGAWA, GUSTAVO HENRIQUE BOFF · 2013 to 2015
$1.2M
A Novel Cell-Based Assay to Identify Small Molecules for B -GalactocerebrosidaseR03MH098689 · NIMH · JOHNS HOPKINS UNIVERSITY · PI MAEGAWA, GUSTAVO HENRIQUE BOFF · 2012 to 2013
$80k
NIMH NIH HHS 1R03MH098689NIMH NIH HHS R03 MH098689NINDS NIH HHS 1R01NS079655NINDS NIH HHS R01 NS079655
6 · The paper itself

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.

Indexed as

AllelesBlood-Brain BarrierCerebroside-SulfataseEnzyme ReactivatorsGenetic TherapyHematopoietic Stem Cell TransplantationHumansLeukodystrophy, MetachromaticCerebroside-SulfataseEnzyme Reactivatorsarylsulfatase Aenzyme enhancement therapyenzyme replacement therapygene therapymetachromatic leukodystrophysmall molecules

Identifiers

PMID23966770
PMCPMC3743609
OpenAlexW2091739816

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

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.