ArticleScientific reports2017
Connecting myelin-related and synaptic dysfunction in schizophrenia with SNP-rich gene expression hubs.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed.
- Prenatal methadone exposure selectively alters protein expression in primary motor cortex: Implications for synaptic function.Frontiers in pharmacology · 2023Article
- Coexpression of the discoidin domain receptor 1 gene with oligodendrocyte-related and schizophrenia risk genes in the developing and adult human brain.Brain and behavior · 2021Article
- Dentate gyrus volume deficit in schizophrenia.Psychological medicine · 2020Article
- Microglial Homeostasis Requires Balanced CSF-1/CSF-2 Receptor Signaling.Cell reports · 2020Article
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Abstract
Combining genome-wide mapping of SNP-rich regions in schizophrenics and gene expression data in all brain compartments across the human life span revealed that genes with promoters most frequently mutated in schizophrenia are expression hubs interacting with far more genes than the rest of the genome. We summed up the differentially methylated "expression neighbors" of genes that fall into one of 108 distinct schizophrenia-associated loci with high number of SNPs. Surprisingly, the number of expression neighbors of the genes in these loci were 35 times higher for the positively correlating genes (32 times higher for the negatively correlating ones) than for the rest of the ~16000 genes. While the genes in the 108 loci have little known impact in schizophrenia, we identified many more known schizophrenia-related important genes with a high degree of connectedness (e.g. MOBP, SYNGR1 and DGCR6), validating our approach. Both the most connected positive and negative hubs affected synapse-related genes the most, supporting the synaptic origin of schizophrenia. At least half of the top genes in both the correlating and anti-correlating categories are cancer-related, including oncogenes (RRAS and ALDOA), providing further insight into the observed inverse relationship between the two diseases.
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