Neuropsychological Functioning in Bipolar Disorder and Schizophrenia

Schretlen, David J.; Cascella, Nicola G.; Meyer, Stephen M.; Kingery, Lisle R.; Testa, S. Marc; Munro, Cynthia A.; Pulver, Ann E.; Rivkin, Paul; Rao, Vani; Diaz-Asper, Catherine; Dickerson, Faith; Yolken, Robert H.; Pearlson, Godfrey D.

doi:10.1016/j.biopsych.2006.09.025

Cited by 234 publications

(176 citation statements)

References 52 publications

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“…32 However, owing to the limitations of using postmortem brain sections, future studies examining the consequences of these alterations to DA signalling and behaviour are required. Furthermore, it is interesting to note that patients with BD and schizophrenia had similar alterations in our study, which is consistent with the results of previous studies showing extensive overlap between these 2 disorders, including cognitive deficits, 33 genetic alterations, 34 changes in brain morphology 35 and oxidative stress. 36 Our results also showed that patients who are not prescribed antidepressants have lower TH and 3NT FRET than controls.…”

Section: Discussionsupporting

confidence: 92%

Oxidation and nitration in dopaminergic areas of the prefrontal cortex from patients with bipolar disorder and schizophrenia

Kim

Andreazza

Yeung

et al. 2014

J Psychiatry Neurosci

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IntroductionBipolar disorder (BD) is characterized by recurrent episodes of mania/hypomania and depression, affects 1.5% of the population, and is associated with high morbidity and mortality. 1 The pathophysiology of BD is linked to a number of factors, including neurotransmitter imbalance, oxidative stress and genetic causes.2 Increased oxidative stress, which could result in oxidative and nitrosative damage to biomolecules, 3 is a consistent finding in patients with BD. For example, mitochondrial dysfunction and decreased expression of genes of the electron transport chain, particularly that of complex I, are reported in patients with BD. 4,5 Decreased efficiency of the electron transport chain could result in increased production of reactive oxygen species (ROS).3 Moreover, increased levels of carbonyl groups, 3-nitrotyrosine (3NT) and decreased levels of antioxidants, such as glutathione, are all reported in patients with BD. [6][7][8][9] It is widely held that dysregulation of the dopamine (DA) system is important in BD, where high levels of DA are thought to underlie mania, a defining feature of the disorder.10 Increasing synaptic DA levels with amphetamine and Levodopa (L-dopa) produces mania-like behaviour, 10,11 and antipsychotics, which act in part by blocking DA receptors, Background: Increased oxidative stress is strongly implicated in bipolar disorder (BD), where protein oxidation, lipid peroxidation and oxidative damage to DNA have been consistently reported. High levels of dopamine (DA) in mania are also well-recognized in patients with BD, and DA produces reactive oxygen species and electron-deficient quinones that can oxidize proteins when it is metabolized. Methods: Using immunohistochemistry and acceptor photobleaching Förster resonance energy transfer (FRET), we examined oxidation and nitration of areas immunoreactive for the DA transporter (DAT) and tyrosine hydroxylase (TH) in the postmortem prefrontal cortex from patients with BD, schizophrenia and major depression as well as nonpsychiatric controls. Results: We found increased oxidation of DAT-immunoreactive regions in patients with BD (F 3,48 = 6.76, p = 0.001; Dunnett post hoc test p = 0.001) and decreased nitration of THimmunoreactive regions in both patients with BD (F 3,45 = 3.10, p = 0.036; Dunnett post hoc test p = 0.011) and schizophrenia (p = 0.027). On the other hand, we found increased global levels of oxidation in patients with BD (F 3,44 = 6.74, p = 0.001; Dunnett post hoc test p = 0.001) and schizophrenia (p = 0.020), although nitration levels did not differ between the groups (F 3,46 = 1.75; p = 0.17). Limitations: Limitations of this study include the use of postmortem brain sections, which may have been affected by factors such as postmortem inter val and antemortem agonal states, although demographic factors and postmortem interval were accounted for in our statistical analysis. Conclusion: These findings suggest alterations in levels of protein oxidation and nitration in DA-rich regions of the prefrontal cortex in pati...

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Section: Discussionsupporting

confidence: 92%

Oxidation and nitration in dopaminergic areas of the prefrontal cortex from patients with bipolar disorder and schizophrenia

Kim

Andreazza

Yeung

et al. 2014

J Psychiatry Neurosci

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“…42,43 In that respect, in five SZ kindreds of Celtic origin that were affected with language impairment or dyslexia, Bartlett et al 44 observed a parametric multipoint lod score of 3.92 with that cognitive impairment in a region of 13q that may overlap the present findings. As neurocognitive impairments have been shown to be shared by patients with SZ or BP, 45 and their unaffected relatives, 46,47 cognitive intermediate phenotypes might help to investigate further the mechanisms involved in chromosome 13q. 42 Also, the concurrent investigation of SZ and BP within the same study may bring advantages to modeling the disease, having in mind the probable joint implications of several susceptibility genes and of epigenetic effects involving environmental factors the nature and timing of which may contribute to explain commonalities as well as specificities in mechanisms underlying psychiatric disorders.…”

Section: Discussionmentioning

confidence: 99%

Chromosome 13q13–q14 locus overlaps mood and psychotic disorders: the relevance for redefining phenotype

et al. 2009

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The nosology of major psychoses is challenged by the findings that schizophrenia (SZ) and bipolar disorder (BP) share several neurobiological, neuropsychological and clinical phenotypic characteristics. Moreover, several vulnerability loci or genes may be common to the two DSM disorders. We previously reported, in a sample of 21 kindreds (sample 1), a genome-wide suggestive linkage in 13q13 -q14 with a common locus (CL) phenotype that crossed the diagnostic boundaries by combining SZ, BP and schizoaffective disorders. Our objectives were to test phenotype specificity in a separate sample (sample 2) of 27 kindreds from Eastern Quebec and to also analyze the combined sample of 48 kindreds (1274 family members). We performed nonparametric and parametric analyses and tested as phenotypes: SZ alone, BP alone, and a CL phenotype. We replicated in sample 2 our initial finding with CL with a maximum NPL pair score of 3.36 at D13S1272 (44 Mb), only 2.1 Mb telomeric to our previous maximum result. In the combined sample, the peak with CL was at marker D13S1297 (42.1 Mb) with a NPL pair score reaching 5.21, exceeding that obtained in each sample and indicating consistency across the two samples. Our data suggest a susceptibility locus in 13q13-q14 that is shared by schizophrenia and mood disorder. That locus would be additional to another well documented and more distal 13q locus where the G72/G30 gene is mapped.

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“…In other words, the relative severity of impairments across different cognitive domains tends to be very similar in bipolar disorder, psychotic major depression and schizoaffective disorders as compared to schizophrenia (e.g., 104,105,109,114).…”

Section: Cognition Across Psychotic Disordersmentioning

confidence: 99%

Cognitive impairments in psychotic disorders: common mechanisms and measurement

2014

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Decades of research have provided robust evidence of cognitive impairments in psychotic disorders. Individuals with schizophrenia appear to be impaired on the majority of neuropsychological tasks, leading some researchers to argue for a "generalized deficit", in which the multitude of cognitive impairments are the result of a common neurobiological source. One such common mechanism may be an inability to actively represent goal information in working memory as a means to guide behavior, with the associated neurobiological impairment being a disturbance in the function of the dorsolateral prefrontal cortex. Here, we provide a discussion of the evidence for such impairment in schizophrenia, and how it manifests in domains typically referred to as cognitive control, working memory and episodic memory. We also briefly discuss cognitive impairment in affective psychoses, reporting that the degree of impairment is worse in schizophrenia than in bipolar disorder and psychotic major depression, but the profile of impairment is similar, possibly reflecting common mechanisms at the neural level. Given the recent release of the DSM-5, we end with a brief discussion on assessing cognition in the context of diagnosis and treatment planning in psychotic disorders.

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Neuropsychological Functioning in Bipolar Disorder and Schizophrenia

Abstract: Background-Some patients with bipolar disorder (BD) demonstrate neuropsychological deficits even when stable. However, it remains unclear whether these differ qualitatively from those seen in schizophrenia (SZ).

Cited by 234 publications

References 52 publications

Oxidation and nitration in dopaminergic areas of the prefrontal cortex from patients with bipolar disorder and schizophrenia

Oxidation and nitration in dopaminergic areas of the prefrontal cortex from patients with bipolar disorder and schizophrenia

Chromosome 13q13–q14 locus overlaps mood and psychotic disorders: the relevance for redefining phenotype

Cognitive impairments in psychotic disorders: common mechanisms and measurement

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