Different trait markers for schizophrenia and bipolar disorder: a neurocognitive approach

Kéri, Szabolcs; Kelemen, Ogúz; Benedek, György; Janka, Zoltán

doi:10.1017/s0033291701004068

Cited by 195 publications

(133 citation statements)

References 35 publications

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“…Siblings of patients with BD or schizophrenia were impaired relative to controls on the long delay components of a verbal memory test, but performed at control levels on other cognitive domains, including a spatial working memory task. 169 Another group compared working memory and explicit memory of first-degree relatives of patients with BD type I and II and controls unrelated to patients with BD. Although the groups preformed at the same level on a picture learning task, the firstdegree relatives of patients with BD were impaired on the recall and recognition tasks of a verbal learning task in comparison to controls.…”

Section: Cognitive Endophenotypesmentioning

confidence: 99%

The phenotypes of bipolar disorder: relevance for genetic investigations

2005

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The search for susceptibility genes for bipolar disorder (BD) depends on appropriate definitions of the phenotype. In this paper, we review data on diagnosis and clinical features of BD that could be used in genetic studies to better characterize patients or to define homogeneous subgroups. Clinical symptoms, long-term course, comorbid conditions, and response to prophylactic treatment may define groups associated with more or less specific loci. One such group is characterized by symptoms of psychosis and linkage to 13q and 22q. A second group includes mainly bipolar II patients with comorbid panic disorder, rapid mood switching, and evidence of chromosome 18 linkage. A third group comprises typical BD with an episodic course and favourable response to lithium prophylaxis. Reproducibility of cognitive deficits across studies raises the possibility of using cognitive profiles as endophenotypes of BD, with deficits in verbal explicit memory and executive function commonly reported. Brain imaging provides a more ambiguous data set consistent with heterogeneity of the illness. Keywords: bipolar disorder; genetics; endophenotype; neurocognitive function; brain imaging Bipolar disorder (BD) has a genetic basis with heritability of at least 80%. 1 A number of studies have attempted to map the susceptibility loci giving evidence of linkage in multiple genomic regions. In particular, findings in 4p, 4q, 8q, 10p, 12q24, 13q, 18p, 18q, 21q, and 22q have been supported by more than one study. [2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19] However, these studies have not identified any specific genes, and a recent metaanalysis of available genome scans showed no regions with a conclusive evidence of linkage. 20 The relatively slow progress of gene-mapping efforts is often explained by the 'complex' nature of the illness and of the genotype-phenotype relation. The complexity most likely includes heterogeneity, interactions of multiple loci, incomplete penetrance, as well as phenotypes resulting from environmental effects-either alone or in interaction with the genetic predisposition. The goal of psychiatric genetic research is identification of (heritable) variations in DNA sequence or function that influence behaviour or give rise to mental illness. By definition, in complex (multifactorial) traits, this link is not unique and specific. That is, a particular change in gene sequence does not necessarily lead to a specific behaviour, and similar behaviours (symptoms) may be due to distinct (sets of) genes. Moreover, we must consider the possibility that the path between the genotype and behaviour is not unidirectional. Emerging examples point not only to general effects of environment, for instance stress, on behaviour, but also to specific behaviours influencing gene function that can be transmitted onto the next generation. 21 No single method is considered clearly superior in identifying susceptibility genes for complex traits such as BD. Most researchers agree that a combination of strategies is most lik...

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Section: Cognitive Endophenotypesmentioning

confidence: 99%

The phenotypes of bipolar disorder: relevance for genetic investigations

2005

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“…Studies have shown the deficit to be stable over time in people with schizophrenia 3,4 and not an epiphenomenon of antipsychotic medications. [5][6][7] Researchers have also found both remitted schizophrenia patients 7 and healthy first-degree biological relatives of schizophrenia patients [8][9][10][11] to have visual percepts that are unusually vulnerable to a subsequent masking stimulus.…”

Section: Introductionmentioning

confidence: 99%

Fragile Early Visual Percepts Mark Genetic Liability Specific to Schizophrenia

Sponheim

Sass

Noukki

et al. 2012

Schizophrenia Bulletin

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Disruption of visual percepts by a subsequent stimulus (ie, backward masking) has been consistently noted in schizophrenia, with some evidence that this fragility in early perception is present in people with genetic liability for the disorder. Given the potential of backward masking paradigms to mark neural processes that confer risk for schizophrenia, it is important to test the diagnostic specificity of abnormalities in visual perception. To more fully assess whether masking visual stimuli reveals a marker of genetic liability (ie, endophenotype) specific to schizophrenia, we tested 44 people with the disorder, 29 people with bipolar disorder, 56 first-degree biological relatives of people with schizophrenia, 26 first-degree biological relatives of people with bipolar disorder, and 43 nonpsychiatric control participants using a magnocellular-biased visual backward masking procedure that included target-to-mask onset asynchronies ranging from 0 to 80 ms. Relatives of people with schizophrenia who were without schizophrenia spectrum disorders exhibited impaired performance compared with nonpsychiatric control participants and relatives of people with bipolar disorder when a visual mask interrupted early perception (eg, 27 ms). A similar vulnerability of early processes was noted in people with schizophrenia, yet they also had impaired performance when masks occurred at later time points (ie, 80 ms). Performance deficits were not attributable to intellectual function, measures of attention and memory, symptomatology, or medication dosage. Bipolar patients and their relatives failed to exhibit deficits on the backward masking task. Fragility of early visual percepts appears to mark genetic liability specific to schizophrenia and may serve as an endophenotype for the disorder.

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“…Two recent meta-analytic studies concluded that too few studies have compared free recall, cued recall, and recognition for the same test in patients with schizophrenia and their relatives (Whyte et al, 2005;Trandafir et al, 2006) such that no firm conclusions can be drawn for the existence or not of retrieval deficits (Trandafir et al, 2006). Some studies have observed deficits in recognition hits among relatives of schizophrenic patients (Lyons et al, 1995), while others have not (Keri et al, 2001;Sponheim et al, 2004). One study showed that relatives performed worse on cued recall compared with controls (Sponheim et al, 2004).…”

Section: Introductionmentioning

confidence: 99%

Verbal recall and recognition in twins discordant for schizophrenia

Erp

Therman

Pirkola

et al. 2008

Psychiatry Research

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The nature, neural underpinnings, and etiology of deficits in verbal declarative memory in patients with schizophrenia remain unclear. To examine the contributions of genes and environment to verbal recall and recognition performance in this disorder, the California Verbal Learning Test was administered to a large population-based Finnish twin sample, which included schizophrenic and schizoaffective patients, their non-ill monozygotic (MZ) and dizygotic (DZ) co-twins, and healthy control twins. Compared with controls, patients and their co-twins showed relatively greater performance deficits on free recall compared with recognition. Intra-pair differences between patients and their non-ill co-twins in hippocampal volume and memory performance were highly positively correlated. These findings are consistent with the view that genetic influences are associated with reduced verbal recall in schizophrenia, but that non-genetic influences further compromise these abnormalities in patients who manifest the full-blown schizophrenia phenotype, with this additional degree of disease-related declarative memory deficit mediated in part by hippocampal pathology.

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Different trait markers for schizophrenia and bipolar disorder: a neurocognitive approach

Cited by 195 publications

References 35 publications

The phenotypes of bipolar disorder: relevance for genetic investigations

The phenotypes of bipolar disorder: relevance for genetic investigations

Fragile Early Visual Percepts Mark Genetic Liability Specific to Schizophrenia

Verbal recall and recognition in twins discordant for schizophrenia

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