There is considerable evidence to suggest that Reelin, an extra-cellular matrix protein mainly expressed by GABAergic inter-neurons, plays a role in the development of schizophrenia. The normal functioning of Reelin is essential for neuronal migration, axonal branching and synaptogenesis throughout the process of brain development. Previous studies have shown that the amount of Reelin is dramatically reduced in the post-mortem brains of patients suffering from schizophrenia, implicating reduced expression of the Reelin gene (RELN) in the aetiology of the disorder.
RELN is located on chromosome 7 and contains a long CpG island in its promoter region. It is estimated that the human genome contains almost 30,000 CpG islands, whose role is to regulate the transcriptional activity of the genes with which they are associated. The methylation of these regulatory CpG sites is associated with the suppression of gene expression.
In an article published in the latest edition of the American Journal of Medical Genetics B, a research team from Harvard Medical School has shown that promoter hypermethylation of the RELN gene could explain the reduced levels of Reelin observed in the brains of schizophrenic patients. Their study found that brain samples from patients diagnosed with schizophrenia had increased DNA methylation of several CpG sites located in the RELN promoter regulatory region. Furthermore, the expression of the RELN gene in their brain samples was strongly correlated with the degree of DNA methylation, suggesting that promoter methylation is responsible for the silencing of RELN expression in schizophrenia.
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