Network Hypoactivity in ALG13-CDG: Disrupted Developmental Pathways and E/I Imbalance as Early Drivers of Neurological Features in CDG

Our study reveals that ALG13-CDG is a disorder of brain-specific hypoglycosylation that disrupts key neurodevelopmental pathways and destabilizes cortical network function. Through integrated multiomic and functional analyses, we identify early network hypoactivity, mistimed neuronal maturation, and evolving E/I imbalance that progresses to compensatory hyperexcitability, providing a mechanistic basis for seizure vulnerability. These findings redefine ALG13-CDG as disorders of cortical network instability, offering a new framework for targeted therapeutic intervention.

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Publication Details

Journal
Cells
Published
2026-01-14
DOI
https://doi.org/10.3390/cells15020147
Primary Topic
Glycosylation and Glycoproteins Research
Type
article
Field-Weighted Citation Impact
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article

Network Hypoactivity in ALG13-CDG: Disrupted Developmental Pathways and E/I Imbalance as Early Drivers of Neurological Features in CDG

Seul Kee Byeon, Eva Morava, Lyndsay E.A. Young, Akhilesh Pandey et al.
Cells
Glycosylation and Glycoproteins Research
article

Network Hypoactivity in ALG13-CDG: Disrupted Developmental Pathways and E/I Imbalance as Early Drivers of Neurological Features in CDG

Seul Kee Byeon, Eva Morava, Lyndsay E.A. Young, Akhilesh Pandey, Rameen Shah, Graeme Preston, Richard R. Drake, Ronald F. Hrstka, Sahar A. Sabry, Alexia King, T. Kozicz, Ibrahim Shammas, Silvia Radenkovic, Jisha Chandran, Nathan P. Staff, Debra Smith, Sean Sloan, Charlotte Bleukx, Rohit Budhhraja
article en

Abstract

Our study reveals that ALG13-CDG is a disorder of brain-specific hypoglycosylation that disrupts key neurodevelopmental pathways and destabilizes cortical network function. Through integrated multiomic and functional analyses, we identify early network hypoactivity, mistimed neuronal maturation, and evolving E/I imbalance that progresses to compensatory hyperexcitability, providing a mechanistic basis for seizure vulnerability. These findings redefine ALG13-CDG as disorders of cortical network instability, offering a new framework for targeted therapeutic intervention.

CellsVol. 15(2)
Mayo Clinic (US), Emory University (US), Medical University of South Carolina (US), Manipal Academy of Higher Education (IN), Utrecht University (NL), WinnMed (US), University Medical Center Utrecht (NL), Stony Brook School (US), National Human Genome Research Institute (US), MUSC Hollings Cancer Center (US), Mayo Clinic in Arizona (US), Mayo Clinic in Florida (US), Institute of Bioinformatics (IN), Stony Brook University (US), University of Pecs (HU), Icahn School of Medicine at Mount Sinai (US)
Openalex Percentile: Top 88%
Glycosylation and Glycoproteins Research
DOIOpen Access PDFOpenAlex
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Network Hypoactivity in ALG13-CDG: Disrupted Developmental Pathways and E/I Imbalance as Early Drivers of Neurological Features in CDG — Seul Kee Byeon, Eva Morava, et al. · Cells (2026) | TGRS Research Map | TGRS