Evidence map›Paper›PMID 25846372›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2015

Sialylation regulates brain structure and function.

Seung-Wan Yoo, Mary G Motari, Keiichiro Susuki, Jillian Prendergast, Andrea Mountney, Andres Hurtado, Ronald L Schnaar

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed, 1 pooled it
3.5field-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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

55 citing papers in PubMed, 1 synthesis or guideline pooled it, 100 citations in OpenAlex.

  1. Mental health dished up-the use of iPSC models in neuropsychiatric research.Journal of neural transmission (Vienna, Austria : 1996) · 2020
    Pooled it
  2. Article
  3. Rare-Variant Burden across Lysosomal Genes Implicates Sialylation and Ganglioside Metabolism in Parkinson's Disease.Movement disorders : official journal of the Movement Disorder Society · 2026
    Article
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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

7 authors at 4 institutions in 1 country.

Seung-Wan Yoo*Department of Pharmacology and Molecular Sciences, Department of Neurology, and Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA; Department of Neuroscience, Baylor College of Medicine, Houston, Texas, USA; Brain Trauma Neuroprotection and Neurorestoration Branch, Center for Military Psychiatry and Neuroscience, Walter Reed Army Institute of Research, Silver Spring, Maryland, USA; and International Center for Spinal Cord Injury, Hugo W. Moser Research Institute, Kennedy Krieger, Baltimore, Maryland, USA.
Mary G Motari*Department of Pharmacology and Molecular Sciences, Department of Neurology, and Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA; Department of Neuroscience, Baylor College of Medicine, Houston, Texas, USA; Brain Trauma Neuroprotection and Neurorestoration Branch, Center for Military Psychiatry and Neuroscience, Walter Reed Army Institute of Research, Silver Spring, Maryland, USA; and International Center for Spinal Cord Injury, Hugo W. Moser Research Institute, Kennedy Krieger, Baltimore, Maryland, USA.
Keiichiro Susuki*Department of Pharmacology and Molecular Sciences, Department of Neurology, and Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA; Department of Neuroscience, Baylor College of Medicine, Houston, Texas, USA; Brain Trauma Neuroprotection and Neurorestoration Branch, Center for Military Psychiatry and Neuroscience, Walter Reed Army Institute of Research, Silver Spring, Maryland, USA; and International Center for Spinal Cord Injury, Hugo W. Moser Research Institute, Kennedy Krieger, Baltimore, Maryland, USA.
Jillian Prendergast*Department of Pharmacology and Molecular Sciences, Department of Neurology, and Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA; Department of Neuroscience, Baylor College of Medicine, Houston, Texas, USA; Brain Trauma Neuroprotection and Neurorestoration Branch, Center for Military Psychiatry and Neuroscience, Walter Reed Army Institute of Research, Silver Spring, Maryland, USA; and International Center for Spinal Cord Injury, Hugo W. Moser Research Institute, Kennedy Krieger, Baltimore, Maryland, USA.
Andrea Mountney*Department of Pharmacology and Molecular Sciences, Department of Neurology, and Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA; Department of Neuroscience, Baylor College of Medicine, Houston, Texas, USA; Brain Trauma Neuroprotection and Neurorestoration Branch, Center for Military Psychiatry and Neuroscience, Walter Reed Army Institute of Research, Silver Spring, Maryland, USA; and International Center for Spinal Cord Injury, Hugo W. Moser Research Institute, Kennedy Krieger, Baltimore, Maryland, USA.
Andres Hurtado*Department of Pharmacology and Molecular Sciences, Department of Neurology, and Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA; Department of Neuroscience, Baylor College of Medicine, Houston, Texas, USA; Brain Trauma Neuroprotection and Neurorestoration Branch, Center for Military Psychiatry and Neuroscience, Walter Reed Army Institute of Research, Silver Spring, Maryland, USA; and International Center for Spinal Cord Injury, Hugo W. Moser Research Institute, Kennedy Krieger, Baltimore, Maryland, USA.
Ronald L Schnaar*Department of Pharmacology and Molecular Sciences, Department of Neurology, and Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA; Department of Neuroscience, Baylor College of Medicine, Houston, Texas, USA; Brain Trauma Neuroprotection and Neurorestoration Branch, Center for Military Psychiatry and Neuroscience, Walter Reed Army Institute of Research, Silver Spring, Maryland, USA; and International Center for Spinal Cord Injury, Hugo W. Moser Research Institute, Kennedy Krieger, Baltimore, Maryland, USA schnaar@jhu.edu.
Johns Hopkins University · USJohns Hopkins Medicine · USBaylor College of Medicine · USWalter Reed Army Institute of Research · US

Funding

BIOCHEMISTRY, CELLULAR AND MOLECULAR BIOLOGY PROGRAMT32GM007445 · NIGMS · JOHNS HOPKINS UNIVERSITY · PI GREEN, RACHEL · 1985 to 2021
$24.1M
Complex Carbohydrates in Neuronal Cell FunctionR37NS037096 · NINDS · JOHNS HOPKINS UNIVERSITY · PI SCHNAAR, RONALD L · 2005 to 2011
$2.8M
COMPLEX CARBOHYDRATES IN NEURONAL CELL FUNCTIONR01NS037096 · NINDS · JOHNS HOPKINS UNIVERSITY · PI SCHNAAR, RONALD L · 1997 to 2004
$1.9M
Targeting Endogenous Inhibitors to Enhance Spinal Axon Regeneration After InjuryR01NS057338 · NINDS · JOHNS HOPKINS UNIVERSITY · PI SCHNAAR, RONALD L · 2008 to 2012
$1.9M
NIGMS NIH HHS T32 GM007445NINDS NIH HHS NS037096NINDS NIH HHS NS057338NINDS NIH HHS R01 NS037096NINDS NIH HHS R01 NS057338NINDS NIH HHS R37 NS037096
6 · The paper itself

Abstract

Every cell expresses a molecularly diverse surface glycan coat (glycocalyx) comprising its interface with its cellular environment. In vertebrates, the terminal sugars of the glycocalyx are often sialic acids, 9-carbon backbone anionic sugars implicated in intermolecular and intercellular interactions. The vertebrate brain is particularly enriched in sialic acid-containing glycolipids termed gangliosides. Human congenital disorders of ganglioside biosynthesis result in paraplegia, epilepsy, and intellectual disability. To better understand sialoglycan functions in the nervous system, we studied brain anatomy, histology, biochemistry, and behavior in mice with engineered mutations in St3gal2 and St3gal3, sialyltransferase genes responsible for terminal sialylation of gangliosides and some glycoproteins. St3gal2/3 double-null mice displayed dysmyelination marked by a 40% reduction in major myelin proteins, 30% fewer myelinated axons, a 33% decrease in myelin thickness, and molecular disruptions at nodes of Ranvier. In part, these changes may be due to dysregulation of ganglioside-mediated oligodendroglial precursor cell proliferation. Neuronal markers were also reduced up to 40%, and hippocampal neurons had smaller dendritic arbors. Young adult St3gal2/3 double-null mice displayed impaired motor coordination, disturbed gait, and profound cognitive disability. Comparisons among sialyltransferase mutant mice provide insights into the functional roles of brain gangliosides and sialoglycoproteins consistent with related human congenital disorders.

Indexed as

AnimalsAstrocytesBehavior, Animalbeta-Galactoside alpha-2,3-SialyltransferaseBrainDemyelinating DiseasesGangliosidesHumansMiceMice, Inbred C57BLMice, KnockoutMice, Mutant StrainsMicrogliaModels, AnimalMutant ProteinsNerve Tissue Proteinsbeta-Galactoside alpha-2,3-SialyltransferaseGangliosidesMutant ProteinsNerve Tissue ProteinsSialic AcidsSialoglycoproteinsSialyltransferasesanimal modelsbehaviorgangliosidesmyelinoligodendrocyte precursor cells

Identifiers

PMID25846372
PMCPMC4478807
OpenAlexW2010951220

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.