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Related Concept Videos

Autism Spectrum Disorder01:19

Autism Spectrum Disorder

38
Autism spectrum disorder (ASD) is a neurodevelopmental condition marked by persistent deficits in social communication and interaction alongside restrictive and repetitive behaviors or interests. ASD is sometimes accompanied by intellectual impairment.
These core symptoms manifest differently among individuals, ranging from mild to severe. The disorder's complexity extends beyond its clinical presentation, encompassing a diverse range of biological, cognitive, and sociocultural influences.
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What is Metabolism?00:52

What is Metabolism?

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Hypometabolism in Autism Spectrum Disorder: Insights from Brain and Blood Transcriptomics.

Rami Balasubramanian1, Debayan Saha1, Ananya Arun1

  • 1Centre for Computational Natural Sciences and Bioinformatics, International Institute of Information Technology, Hyderabad, 500032, India.

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Autism spectrum disorder (ASD) involves metabolic dysfunction, with key pathways downregulated in the brain and blood. This suggests hypometabolism contributes to ASD, offering targets for new therapies.

Keywords:
Autism spectrum disorderBrain and blood transcriptomicsMetabolic dysregulation

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Area of Science:

  • Neuroscience
  • Metabolomics
  • Genomics

Background:

  • Autism spectrum disorder (ASD) is a neurodevelopmental condition.
  • Metabolic dysfunctions are increasingly recognized in ASD pathophysiology.
  • Understanding these metabolic alterations is crucial for developing effective interventions.

Purpose of the Study:

  • To investigate metabolic alterations in ASD using transcriptomic data from brain and blood.
  • To identify specific metabolic pathways and genes associated with ASD.
  • To explore cell-specific metabolic changes in the ASD brain.

Main Methods:

  • Analysis of transcriptomic data from prefrontal cortex (bulk and single-nucleus) and peripheral blood mononuclear cells (PBMC).
  • Assessment of metabolic activity based on gene expression profiles.
  • Identification of differentially expressed genes and pathways in ASD versus typically developing individuals.

Main Results:

  • Significant downregulation of glycolysis, TCA cycle, and oxidative phosphorylation in ASD, indicating hypometabolism.
  • Dysregulation observed in lipid, vitamin, amino acid, and heme metabolism.
  • Distinct metabolic profiles identified in astrocytes, oligodendrocytes, excitatory neurons, and interneurons in ASD brains.
  • PBMC gene expression data revealed specific metabolic pathways and genes differentiating ASD patients.

Conclusions:

  • Consistent metabolic dysfunction observed across brain and blood samples in ASD.
  • Hypometabolism and dysregulated metabolic pathways are implicated in ASD pathophysiology.
  • Findings provide a foundation for developing targeted metabolic therapies for ASD.