ReviewPhilosophical transactions of the Royal Society of London. Series B, Biological sciences2003
Neurobiology and cellular pathogenesis of glycolipid storage diseases.
Review in Philosophical transactions of the Royal Society of London. Series B, Biological sciences, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 50 citations in OpenAlex.
- Review
- GM1 Gangliosidosis: Mechanisms and Management.The application of clinical genetics · 2021Review
- Gangliosides of the Vertebrate Nervous System.Journal of molecular biology · 2016Review
- Mucopolysaccharidosis type I: current knowledge on its pathophysiological mechanisms.Metabolic brain disease · 2012Review
- Elevation of GM2 ganglioside during ethanol-induced apoptotic neurodegeneration in the developing mouse brain.Journal of neurochemistry · 2012Article
- Lipid rafts and Alzheimer's disease: protein-lipid interactions and perturbation of signaling.Frontiers in physiology · 2012Article
- Endosomal/lysosomal processing of gangliosides affects neuronal cholesterol sequestration in Niemann-Pick disease type C.The American journal of pathology · 2011Article
- Cerebellar alterations and gait defects as therapeutic outcome measures for enzyme replacement therapy in α-mannosidosis.Journal of neuropathology and experimental neurology · 2011Article
- Clinical aspects of neuropathic lysosomal storage disorders.Journal of inherited metabolic disease · 2010Review
- Cell-cell signaling drives the evolution of complex traits: introduction-lung evo-devo.Integrative and comparative biology · 2009Article
- Enzyme replacement improves ataxic gait and central nervous system histopathology in a mouse model of metachromatic leukodystrophy.Molecular therapy : the journal of the American Society of Gene Therapy · 2009Article
- Pathogenic cascades in lysosomal disease-Why so complex?Journal of inherited metabolic disease · 2009Review
- Secondary lipid accumulation in lysosomal disease.Biochimica et biophysica acta · 2009Review
- MR imaging and proton spectroscopy of neuronal injury in late-onset GM2 gangliosidosis.AJNR. American journal of neuroradiology · 2005Article
- Isopentenyl-diphosphate isomerase is essential for viability of Caenorhabditis elegans.Molecular genetics and genomics : MGG · 2005Article
- Future perspectives for glycolipid research in medicine.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2003Review
- A historical perspective of the glycosphingolipids and sphingolipidoses.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2003Article
- Substrate reduction therapy of glycosphingolipid storage disorders.Journal of inherited metabolic diseaseArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Disorders of lysosomal metabolism often involve the accumulation of specific types of glycolipid, particularly gangliosides, because of either degradative failure or other currently unknown mechanisms. Although the precise role of gangliosides in cells remains enigmatic, the presence of specific abnormalities secondary to ganglioside accumulation in lysosomal diseases has suggested important biological functions. Chief among these is the growth of new dendrites on particular classes of mature neurons secondary to an increase in GM2 ganglioside. That GM2 has also been shown to be elevated in normal immature neurons coincident with dendritic sprouting provides a compelling argument that this ganglioside plays a role in dendritic initiation. This discovery has led to the search for other regulators of dendritic differentiation that may in some way be linked to the expression and/or function of GM2 ganglioside. Principal candidates that have emerged include tyrosine kinase receptors, small GTPases and calcium/calmodulin-dependent protein kinase II. Understanding the mechanism underlying ectopic dendritogenesis in lysosomal diseases can be expected to generate significant insight into the control of dendritic plasticity in normal brain. The detrimental aspects of ganglioside accumulation in storage diseases as well as the potential link between gangliosides and dendritogenesis also provide a strong rationale for developing pharmacological means to manipulate ganglioside expression in neurons.
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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.