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Modeling the genetics of schizophrenia – the curse of plentitude?

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Author(s): Barbara K. Lipska

Journal: Neuropsychiatria i Neuropsychologia
ISSN 1896-6764

Volume: 2;
Issue: 2;
Start page: 51;
Date: 2007;
Original page

Keywords: modeling the genetics schizophrenia | DISC1

ABSTRACT
Rapidly growing knowledge about the neurobiology andgenetics of schizophrenia has stimulated new interest inanimal models, which are used to dissect the molecularmechanisms of pathophysiological abnormalities inschizophrenia and create more effective therapies. Theconcepts about how to approach animal modeling of thiscomplex, multifactorial (i.e., involving multiple genesand a variety of epigenetic causes) neuropsychiatricdisorder have been evolving over years and reflect thechanging ideas about the etiology and the mechanism ofthe illness (Lipska and Weinberger 2000; Chen et al.2006). These past approaches included pharmacologicalmanipulations of dopamine and glutamate systems,thought to be in the center of the neurotransmitterimbalance in schizophrenia and the main culprits in thepsychotic symptoms and cognitive impairments (Costalland Naylor 1995). Subsequent concepts focused ondisruptions of early brain development to address theevidence that the disorder has a neurodevelopmentalorigin; the onset of schizophrenia is typically inadolescence or early adulthood and early childhood is notnormal in many cases (Lipska and Weinberger 2000;Moore et al. 2006). Manipulations of the psychosocialenvironment and induction of stressful conditions havealso been considered as model targets due to the evidencethat stress is involved in precipitating the illness (Joneset al. 1992). Most recently, however, a new generationof models based on the breakthroughs in the discoveryof human schizophrenia susceptibility genes have yieldedthe most fascinating results. Although they brought usa bit closer to understanding the functions of some“faulty” genes, they have also raised more questions aboutthe functions of the putative susceptibility genes andtheir role in the human disorder.
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