Animal models of schizophrenia are important for research aimed at developing improved pharmacotherapies. In particular, the cognitive deficits of schizophrenia remain largely refractory to current medications and there is a need for improved medications. We discuss the pathophysiology of schizophrenia and in particular the possible mechanisms underlying the cognitive deficits. We review the current animal models of schizophrenia and discuss the extent to which they meet the need for models reflecting the various domains of the symptomatology of schizophrenia, including positive symptoms, negative symptoms and cognitive symptoms.
Schizophrenia is a debilitating condition with a mean lifetime morbidity risk of approximately 1:100.1 The current diagnosis of schizophrenia is based primarily on DSM IV. Symptoms of schizophrenia have classically been divided into 2 groups: the positive and negative symptoms. The positive symptoms are symptoms added on to normal behaviour or function. For example, psychotic symptoms such as hallucinations, delusions and other thought disorders. The negative symptoms are symptoms subtracted from normal behaviour or function. For example, social withdrawal, blunted affect and lack of motivation. In addition, those suffering from schizophrenia often exhibit other symptoms including aggression and varying degrees of cognitive dysfunction. In the past decade, it has been increasingly appreciated that cognitive deficits are also a core feature of the disorder present from before the onset of the first acute episode of positive symptoms.2 As the cognitive deficits are strongly associated with functional disability and are largely refractory to current medications, the amelioration of cognitive dysfunction has become an important target for psychopharmacological research into improved pharmacotherapies for schizophrenia.
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