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Lipidomics and Transcriptomics in Neurological Diseases
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Spatial Lipidomics Reveals Region-Specific Lipid Remodeling in Scn2a-Deficient Mouse Brain.

Alyssa Moore1, Xiaoling Chen2,3, Emerson Hernly1

  • 1James Tarpo Jr. and Margaret Tarpo Department of Chemistry, Purdue University, West Lafayette, Indiana 47907, United States.

ACS Chemical Neuroscience
|March 30, 2026
PubMed
Summary

Scn2a gene deficiency alters brain lipid profiles in mice, revealing changes in phosphatidylethanolamine levels linked to neurodevelopmental disorders.

Keywords:
epilepsylipidomicsmass spectrometry imagingnano-DESIneurodevelopmental disordersspatial neurobiology

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Area of Science:

  • Neuroscience
  • Biochemistry
  • Analytical Chemistry

Background:

  • Scn2a gene encodes NaV1.2, crucial for neuronal excitability.
  • Scn2a dysfunction is implicated in epilepsy and autism spectrum disorder.
  • Molecular changes in Scn2a deficiency are not well understood.

Purpose of the Study:

  • Investigate regional lipid and metabolite alterations in Scn2a-deficient mouse brains.
  • Utilize nanospray desorption electrospray ionization mass spectrometry imaging (nano-DESI MSI).
  • Compare wild-type (WT) and Scn2a homozygous gene-trap (HOM) mouse brain tissues.

Main Methods:

  • Employed nano-DESI MSI on an Orbitrap mass spectrometer.
  • Performed experiments in positive and negative ionization modes.
  • Conducted region-of-interest (ROI) analysis on three biological replicates per group.

Main Results:

  • Identified altered lipid abundances in HOM mouse brains compared to WT.
  • Observed increased levels of specific phosphatidylethanolamine (PE) lipids (e.g., PE(O-36:5), PE(40:4)) in various brain regions.
  • Detected decreased levels of phosphatidylserine (PS(38:1)) in the cortex, while structural lipids remained unchanged.

Conclusions:

  • Nano-DESI MSI provides comprehensive insights into lipid alterations in Scn2a deficiency.
  • Specific lipid changes may underlie epilepsy and neurodevelopmental disorders associated with Scn2a dysfunction.
  • Findings contribute to understanding the molecular basis of Scn2a-related neurological conditions.