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Related Experiment Video

Updated: Apr 15, 2026

Author Spotlight: Dendritic Cells Maturation Using Sialidases-Based Enzymatic Treatment of the Cell Surface

Author Spotlight: Dendritic Cells Maturation Using Sialidases-Based Enzymatic Treatment of the Cell Surface

Published on: October 20, 2023

Sialylation regulates brain structure and function.

Seung-Wan Yoo¹, Mary G Motari¹, Keiichiro Susuki¹

¹*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.

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology

|April 8, 2015

Summary

Mutations in sialyltransferase genes St3gal2 and St3gal3 cause severe brain defects in mice, including impaired myelin, smaller neurons, and significant cognitive and motor disabilities, mirroring human disorders.

Keywords:

animal models behavior gangliosides myelin oligodendrocyte precursor cells

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Last Updated: Apr 15, 2026

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Published on: October 20, 2023

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Published on: March 12, 2021

Metabolic Glycoengineering of Sialic Acid Using N-acyl-modified Mannosamines

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Published on: November 25, 2017

Area of Science:

Neuroscience
Biochemistry
Glycobiology

Background:

The cell surface features a diverse glycan coat (glycocalyx), crucial for cellular interactions.
Sialic acids, anionic sugars, are abundant in the vertebrate brain as gangliosides, vital for nervous system function.
Congenital disorders affecting ganglioside biosynthesis in humans lead to severe neurological impairments.

Purpose of the Study:

To investigate the role of sialic acids in the nervous system by examining mice with mutations in St3gal2 and St3gal3.
To understand the function of brain gangliosides and sialoglycoproteins in neural development and function.

Main Methods:

Generated and analyzed St3gal2/3 double-null mice with engineered mutations.
Conducted comprehensive studies on brain anatomy, histology, biochemistry, and behavior.
Assessed myelination, neuronal structure, and cognitive and motor functions.

Main Results:

St3gal2/3 double-null mice exhibited significant dysmyelination, including reduced myelin proteins, fewer myelinated axons, and thinner myelin sheaths.
Observed molecular disruptions at nodes of Ranvier and reduced neuronal markers, with smaller hippocampal dendritic arbors.
Double-null mice displayed impaired motor coordination, gait disturbances, and profound cognitive deficits.

Conclusions:

Sialylation mediated by St3gal2 and St3gal3 is critical for proper brain development, myelination, and neuronal structure.
Dysregulation of ganglioside-mediated oligodendroglial precursor cell proliferation contributes to observed neuropathology.
These findings provide insights into the functional roles of brain gangliosides and sialoglycoproteins, consistent with human congenital disorders.