Unravelling the genetic basis of Schizophrenia

被引:2
|
作者
Casey, Clara [1 ,2 ,3 ,4 ]
Fullard, John F. [2 ,3 ,4 ]
Sleator, Roy D. [1 ]
机构
[1] Munster Technol Univ, Dept Biol Sci, Cork, Ireland
[2] Icahn Sch Med Mt Sinai, Ctr Dis Neurogen, New York, NY 10029 USA
[3] Icahn Sch Med Mt Sinai, Dept Psychiat, New York, NY 10029 USA
[4] Icahn Sch Med Mt Sinai, Dept Genet & Genom Sci, New York, NY 10029 USA
关键词
Schizophrenia; Omics technologies; Genetics; Epigenetics; LONG-TERM POTENTIATION; DNA METHYLATION; GLUTAMATE HYPOTHESIS; DOPAMINE HYPOTHESIS; SIGNALING PATHWAYS; REELIN EXPRESSION; OXIDATIVE STRESS; POSTMORTEM BRAIN; OPEN CHROMATIN; NONCODING RNA;
D O I
10.1016/j.gene.2024.148198
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
Neuronal development is a highly regulated mechanism that is central to organismal function in animals. In humans, disruptions to this process can lead to a range of neurodevelopmental phenotypes, including Schizophrenia (SCZ). SCZ has a significant genetic component, whereby an individual with an SCZ affected family member is eight times more likely to develop the disease than someone with no family history of SCZ. By examining a combination of genomic, transcriptomic and epigenomic datasets, large-scale 'omics' studies aim to delineate the relationship between genetic variation and abnormal cellular activity in the SCZ brain. Herein, we provide a brief overview of some of the key omics methods currently being used in SCZ research, including RNAseq, the assay for transposase-accessible chromatin with high-throughput sequencing (ATAC-seq) and highthroughput chromosome conformation capture (3C) approaches (e.g., Hi-C), as well as single-cell/nuclei iterations of these methods. We also discuss how these techniques are being employed to further our understanding of the genetic basis of SCZ, and to identify associated molecular pathways, biomarkers, and candidate drug targets.
引用
收藏
页数:12
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