Article

Barch DM, Ceaser A. Cognition in schizophrenia: core psychological and neural mechanisms. Trends Cogn Sci 16: 27-34

Department of Psychiatry, Washington University in St. Louis, San Luis, Missouri, United States
Trends in Cognitive Sciences (Impact Factor: 21.97). 12/2011; 16(1):27-34. DOI: 10.1016/j.tics.2011.11.015
Source: PubMed

ABSTRACT

The challenge in understanding cognitive impairment in schizophrenia is that people with this illness have deficits in an array of domains. Here, we briefly review evidence regarding the pattern of deficits within three domains: context processing, working memory and episodic memory. We suggest that there may be a common mechanism driving deficits in these domains - an impairment in the ability to actively represent goal information in working memory to guide behavior, a function we refer to as proactive control. We suggest that such deficits in proactive control reflect impairments in dorsolateral prefrontal cortex, its interactions with other brain regions, such as parietal cortex, thalamus and striatum, and the influence of neurotransmitter systems, such as dopamine, GABA and glutamate.

    • "On the other hand, an intriguing finding in psychosis research is that, despite schizophrenia and other psychoses running in families, most affected individuals do not have family history of the illness (Welham et al., 2009). There is now increasing evidence suggesting that cognitive dysfunction is a reliable and stable feature of psychosis (Barch and Ceaser, 2012) and that it predicts psychosocial functioning and functional capacity better than clinical manifestations in schizophrenia patients (Bowie et al., 2008). Moreover, an association between bipolar disorder and cognitive impairment has repeatedly been described even for euthymic patients. "
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    ABSTRACT: Introduction: Phenotype definition of psychotic disorders has a strong impact on the degree of familial aggregation. Nevertheless, the extent to which distinct classification systems affect familial aggregation (ie, familiality) remains an open question. This study was aimed at examining the familiality associated with 4 nosologic systems of psychotic disorders (DSM-IV, ICD-10, Leonhard's classification and a data-driven approach) and their constituting diagnoses in a sample of multiplex families with psychotic disorders. Methods: Participants were probands with a psychotic disorder, their parents and at least one first-degree relative with a psychotic disorder. The sample was made of 441 families comprising 2703 individuals, of whom 1094 were affected and 1709 unaffected. Results: The Leonhard classification system had the highest familiality (h (2) = 0.64), followed by the empirical (h (2) = 0.55), DSM-IV (h (2) = 0.50), and ICD-10 (h (2) = 0.48). Familiality estimates for individual diagnoses varied considerably (h (2) = 0.25-0.79). Regarding schizophrenia diagnoses, Leonhard's systematic schizophrenia (h (2) = 0.78) had the highest familiality, followed by latent class core schizophrenia (h (2) = 0.74), DSM-IV schizophrenia (h (2) = 0.48), and ICD-10 schizophrenia (h (2) = 0.41). Psychotic mood disorders showed substantial familiality across nosologic systems (h (2) = 0.60-0.77). Domains of psychopathology other than reality-distortion symptoms showed moderate familiality irrespective of diagnosis (h (2) = 0.22-0.52) with the deficit syndrome of schizophrenia showing the highest familiality (h (2) = 0.66). Conclusions: While affective psychoses showed relatively high familiality estimates across classification schemes, those of nonaffective psychoses varied markedly as a function of the diagnostic scheme with a narrow schizophrenia phenotype maximizing its familial aggregation. Leonhard's classification of psychotic disorders may be better suited for molecular genetic studies than the official diagnostic systems.
    No preview · Article · Dec 2015 · Schizophrenia Bulletin
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    • "Thus the present findings suggest that the ability to gate intrusive sensory information could protect patients with schizophrenia against hallucinatory behaviors . Although no causal link can be drawn, they demonstrate: (i) the value of research strategies focusing on specific symptoms and their relationships with cognitive impairments in psychiatric disorders (Barch and Ceaser, 2012; Elvevag and Goldberg, 2000), and (ii) the need to target core cognitive impairments such as sensory gating deficits in order to develop new effective strategies against hallucinatory behavior. "

    Full-text · Article · Nov 2015 · Clinical neurophysiology: official journal of the International Federation of Clinical Neurophysiology
    • "In this chapter, we will illustrate the cognitive impairments presently believed to be hallmarks of schizophrenia and the most relevant corresponding tasks suggested to be used in animal models. In particular, the cognitive domains that we will specifically address are executive control, working memory, attention, and social cognition as these are the cognitive functions most frequently found to be altered in patients with schizophrenia (Barch & Ceaser, 2012;Ross et al., 2006). "
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    ABSTRACT: Cognitive impairments, especially in higher order cognitive functions, are core features of schizophrenia. Importantly, despite their early onset, long-lasting presence, and serious impact on the life quality of patients and their families, cognitive deficits are still mostly incurable and their specific causes are still unknown. In this context, mouse/rat models with cautious and well-designed translational valence constitute an invaluable instrument in dissecting the selective nature of schizophrenia-relevant cognitive deficits, including their genetic, environmental, and neuronal/cellular mechanisms. Moreover, these models are also crucial for the implementation of more effective therapeutical strategies. Thus, based on clinical evidence in schizophrenia, here we will specifically address cognitive domains such as executive control, working memory, attention, and social cognition. We first briefly present human tasks commonly used to measure each of these domains; thereafter, we describe relevant equivalent tasks developed and now available for use in rodents.
    No preview · Chapter · Nov 2015
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