Background: Abnormal structural/functional connectivity has been proposed to underlie the pathophysiology of schizophrenia. However, the biochemical basis of abnormal connectivity remains undefined.
Methods: We undertook a shotgun lipidomic analysis of over 700 lipids across 26 lipid subclasses in the frontal cortex of schizophrenia subjects and hippocampus of G72/G30 transgenic mice.
Results: We demonstrate that glycosphingolipids and choline plasmalogens, structural lipid pools in myelin, are significantly elevated in the frontal cortex obtained from patients suffering from schizophrenia and the hippocampus of G72/G30 transgenic mice.
Conclusions: Our data suggest that structural lipid alterations in oligodendrocyte glycosynapses are responsible for dysconnectivity in schizophrenia and that increased expression of G72 protein may play a role in the development of abnormal glycosynapses.
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The primate-specific G72/G30 gene locus has been associated with major psychiatric disorders, such as schizophrenia and bipolar disorder. We have previously generated transgenic mice which carry the G72/G30 locus and express the longest G72 splice variant (LG72) protein encoded by this locus with schizophrenia-related symptoms. Here, we used a multi-omics approach, including quantitative proteomics and metabolomics to investigate molecular alterations in the hippocampus of G72/G30 transgenic (G72Tg) mice.
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Article Synopsis
- Genetic studies have linked the G72/G30 gene locus to schizophrenia and other psychiatric disorders, but the role of its protein, LG72, remains debated.
- Some research suggests that LG72 interacts with D-amino-acid-oxidase, while other studies point to its function related to mitochondria, indicating it may lead to oxidative stress.
- This study identifies mitochondrial methionine-R-sulfoxide reductase B2 (MSRB2) as a specific partner for LG72, suggesting that LG72 plays a role in managing mitochondrial oxidative stress levels.
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