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Multifaceted genomic risk for brain function in schizophrenia.

Jiayu Chen¹, Vince D Calhoun, Godfrey D Pearlson

¹Department of Electrical and Computer Engineering, University of New Mexico, Albuquerque, NM 87131-0001, USA. jchen@mrn.org

|March 24, 2012

Summary

This summary is machine-generated.

This study links genetic variations to brain function abnormalities in schizophrenia (SZ). Specific genetic components correlate with altered brain activity in patients, suggesting complex gene interactions contribute to SZ susceptibility.

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Published on: June 15, 2011

Area of Science:

Neuroscience
Psychiatry
Genetics

Background:

Schizophrenia (SZ) pathophysiology is unclear, prompting research into genetic influences.
Brain imaging endophenotypes offer a valuable approach to study genetic contributions to SZ.

Purpose of the Study:

To identify genomic risk components associated with brain function abnormalities in SZ.
To investigate the association between genetic variations and brain activations in SZ patients.

Main Methods:

Utilized parallel independent component analysis (a multivariate approach).
Analyzed 5157 candidate single nucleotide polymorphisms (SNPs) and functional magnetic resonance imaging (fMRI) data from 92 SZ patients and 116 healthy controls during a sensorimotor task.

Main Results:

A significant correlation (r=0.29; p=2.41 × 10(-5)) was found between a specific fMRI component (precentral and postcentral gyri) and an SNP component.
Higher activation in motor regions correlated with higher loadings of the linked SNP component, involving 253 SNPs.
Identified SNPs linked to genes in GABA, dopamine, neuregulin, and glutamate signaling pathways, suggesting complex genetic interactions.

Conclusions:

The study provides evidence for the complexity of genomic risk in functional brain abnormalities in SZ.
Interactions among SNPs, genes, and multiple neurotransmitter pathways may play a pathological role in SZ susceptibility.