ReviewGlia2021
Mechanisms of demyelination and neurodegeneration in globoid cell leukodystrophy.
Review in Glia, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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
25 citing papers in PubMed, 37 citations in OpenAlex.
- Validating a Human Cell Model of Null Galactosylceramidase (GALC) Enzyme Activity That Recapitulates Krabbe Disease.Journal of inherited metabolic disease · 2026Article
- First reported case of Turner syndrome with Krabbe disease in a child: a case report.Translational pediatrics · 2026Article
- Neurodegenerative Diseases in Children: A Comprehensive Review.International journal of molecular sciences · 2026Review
- In vivo adenine base editing of mutant Galc gene ameliorates Krabbe disease progression.Genome medicine · 2026Article
- Clinical and molecular characterization of Krabbe disease in Iranian patients: case report and literature review.BMC neurology · 2026Review
- A case report of integrating Chinese and Western medicine: A new era in the treatment of late-onset Krabbe disease.Transplantation · 2026Article
- Brain accumulation of lactosylceramide characterizes GALC deficiency in a zebrafish model of Krabbe disease.Brain : a journal of neurology · 2025Article
- Pathologic and Therapeutic Schwann Cells.Cells · 2025Review
- Article
- Broken Balance: Emerging Cross-Talk Between Proteostasis and Lipostasis in Neurodegenerative Diseases.Cells · 2025Review
- Ablation of lipocalin-2 reduces neuroinflammation in a mouse model of Krabbe disease.Scientific reports · 2024Article
- The Effect of Donepezil Hydrochloride in the Twitcher Mouse Model of Krabbe Disease.Molecular neurobiology · 2024Article
- CD8+ T cell depletion prevents neuropathology in a mouse model of globoid cell leukodystrophy.The Journal of experimental medicine · 2023Article
- Article
- rAAV2-Mediated Restoration of GALC in Neural Stem Cells from Krabbe Patient-Derived iPSCs.Pharmaceuticals (Basel, Switzerland) · 2023Article
- Altered plasma membrane abundance of the sulfatide-binding protein NF155 links glycosphingolipid imbalances to demyelination.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Zebra-Sphinx: Modeling Sphingolipidoses in Zebrafish.International journal of molecular sciences · 2023Review
- The endo-lysosomal regulatory protein BLOC1S1 modulates hepatic lysosomal content and lysosomal lipolysis.Biochemical and biophysical research communications · 2023Article
- Globoid Cell Leukodystrophy (Krabbe Disease): An Update.ImmunoTargets and therapy · 2023Review
- Genome Editing Tools for Lysosomal Storage Disorders.Advances in experimental medicine and biology · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Globoid cell leukodystrophy (GLD), also known as Krabbe disease, is a lysosomal storage disorder causing extensive demyelination in the central and peripheral nervous systems. GLD is caused by loss-of-function mutations in the lysosomal hydrolase, galactosylceramidase (GALC), which catabolizes the myelin sphingolipid galactosylceramide. The pathophysiology of GLD is complex and reflects the expression of GALC in a number of glial and neural cell types in both the central and peripheral nervous systems (CNS and PNS), as well as leukocytes and kidney in the periphery. Over the years, GLD has garnered a wide range of scientific and medical interests, especially as a model system to study gene therapy and novel preclinical therapeutic approaches to treat the spontaneous murine model for GLD. Here, we review recent findings in the field of Krabbe disease, with particular emphasis on novel aspects of GALC physiology, GLD pathophysiology, and therapeutic strategies.
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.