Zebrafish as a tool to study schizophrenia-associated copy number variants.
作者： Philip D. Campbell , Michael Granato
DOI: 10.1242/DMM.043877
关键词: Schizophrenia (object-oriented programming) 、 Attention deficit hyperactivity disorder 、 Gene 、 Identification (biology) 、 Behavioural genetics 、 Biology 、 Computational biology 、 Copy-number variation 、 Developmental neurobiology 、 Zebrafish
摘要: Schizophrenia remains one of the most debilitating human neurodevelopmental disorders, with few effective treatments and striking consequences felt by individuals, communities society as a whole. As such, there critical need for further investigation into mechanistic underpinnings schizophrenia so that novel therapeutic targets can be identified. Because is highly heritable disorder, genetic risk factors remain an attractive avenue this research. Given their clear molecular consequences, recurrent microdeletions duplications, or copy number variants (CNVs), represent tractable entry points to elucidating these mechanisms. To date, eight CNVs have been shown significantly increase schizophrenia. Although rodent models exhibit behavioral phenotypes generated, underlying mechanisms largely elusive. Over past decades, zebrafish has emerged powerful vertebrate model led fundamental discoveries in developmental neurobiology genetics. Here, we review attributes make exceptionally well suited investigating individual combinatorial gene contributions CNV-mediated brain dysfunction With conserved genetics neural substrates, ever-expanding imaging toolkit, ability perform high-throughput high-content pharmacologic screens, poised generate deep insights schizophrenia-associated deficits, facilitate identification targets.
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