Differences in cognitive impairment between schizophrenia and bipolar disorder: Considering the role of heterogeneity

Bora, Emre

doi:10.1111/pcn.12410

Cited by 105 publications

(63 citation statements)

References 101 publications

(230 reference statements)

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“…It is also important to note that similar cross diagnostic differences between SCZ and BD have been reported by several previous studies that have examined neurocognition, functional magnetic resonance imaging (fMRI) and prevalence of metabolic syndrome . Studies have reported that patients with SCZ have greater impairment in cognitive functions compared to BD . A recent study has reported decreased volume of the CC (corpus callosum) associated with a lower degree of left hemispherical asymmetry for language in BD which was not replicated in SCZ.…”

Section: Discussionmentioning

confidence: 70%

Retinal vascular abnormalities in schizophrenia and bipolar disorder: A window to the brain

et al. 2019

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Objectives The examination of retinal microvascular abnormalities through fundus photography is currently the best available non‐invasive technique for assessment of cerebral vascular status. Several studies in the last decade have reported higher incidences of adverse cerebrovascular events in Schizophrenia (SCZ) and bipolar disorder (BD). However, retinal microvasculature abnormalities in SCZ and BD have remained under‐explored, and no study has compared this aspect of SCZ and BD till date. Methods Retinal Images of 100 SCZ patients, BD patients, and healthy volunteers each were acquired by trained individuals using a non‐mydriatic camera with a 40‐degree field of view. The retinal images were quantified using a valid semi‐automated method. The average of left and right eye diameters of the venules and arterioles passing through the extended zone between 0.5 and 2 disc diameters from the optic disc were calculated. Results The groups differed significantly with respect to average diameters of both retinal venules (P < 0.001) and retinal arterioles (P < 0.001), after controlling for age and sex. Both SCZ and BD patients had significantly narrower arterioles and wider venules compared to HV. There were also significant differences between SCZ and BD patients; patients with BD had narrower arterioles and wider venules. Conclusion Considering the affordability and easy accessibility of the investigative procedure, retinal microvascular examination could serve as a potential screening tool to identify individuals at risk for adverse cerebrovascular events. The findings of the current study also provide a strong rationale for further systematic examination of retinal vascular abnormalities in SCZ and BD.

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Section: Discussionmentioning

confidence: 70%

Retinal vascular abnormalities in schizophrenia and bipolar disorder: A window to the brain

et al. 2019

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“…The drug × gene × time interactions are significant, indicating cKO mice may bear different sensitivity to methylphenidate from control, although the key point is that there were increases overall, not decreases. We did not detect severe deficits in cognitive tests, and cognition is generally reported to be more severely altered in schizophrenia than bipolar disorder (27,47). Future studies could include more sensitive and sophisticated cognitive function tests.…”

Section: Discussionmentioning

confidence: 86%

“…Cognitive decline is one of the core features of patients with schizophrenia, and may be present, but is usually less prominent, in bipolar disorder (27). We performed Y maze tests (spatial learning and memory), and 1-h and 24-h novel object recognition tests (short-and long-term visual memory).…”

Section: Ank-g Cko Mouse Cortical Pyramidal Neurons Lose Ion Channel mentioning

confidence: 99%

Genetic disruption of ankyrin-G in adult mouse forebrain causes cortical synapse alteration and behavior reminiscent of bipolar disorder

Zhu

Cordner²,

Xiong

et al. 2017

Proc. Natl. Acad. Sci. U.S.A.

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Genome-wide association studies have implicated the ANK3 locus in bipolar disorder, a major human psychotic illness. ANK3 encodes ankyrin-G, which organizes the neuronal axon initial segment (AIS).We generated a mouse model with conditional disruption of ANK3 in pyramidal neurons of the adult forebrain (Ank-G cKO). This resulted in the expected loss of pyramidal neuron AIS voltage-gated sodium and potassium channels. There was also dramatic loss of markers of afferent GABAergic cartridge synapses, resembling the cortical microcircuitry changes in brains from psychotic patients, and suggesting disinhibition. Expression of c-fos was increased in cortical pyramidal neurons, consistent with increased neuronal activity due to disinhibition. The mice showed robust behavioral phenotypes reminiscent of aspects of human mania, ameliorated by antimania drugs lithium and valproate. Repeated social defeat stress resulted in repeated episodes of dramatic behavioral changes from hyperactivity to "depressionlike" behavior, suggestive of some aspects of human bipolar disorder. Overall, we suggest that this Ank-G cKO mouse model recapitulates some of the core features of human bipolar disorder and indicates that cortical microcircuitry alterations during adulthood may be involved in pathogenesis. The model may be useful for studying disease pathophysiology and for developing experimental therapeutics.B ipolar disorder and schizophrenia are major psychiatric disorders. Bipolar patients experience both mania, with elevated mood and activity, and depression (often triggered by stress), with low mood and activity. Bipolar disorder is often uniquely responsive to lithium (Li). Many loci have been identified by genome-wide association studies (GWASs) for schizophrenia (1). By contrast, fewer loci with genome-wide significance have been identified for bipolar disorder (2), with some overlap, suggesting some shared mechanisms.In a recent large GWAS of bipolar disorder (3), the most significant signal was detected at the ANK3 locus. This finding has been replicated in many (if not all) GWASs of bipolar disorder (3-5). The ANK3 locus is also found to be associated, to a lesser extent, with schizophrenia (6, 7).The ANK3 gene encodes ankyrin-G, a large scaffold protein highly expressed in neurons in the brain (8). Three main brainspecific splice variants encode 190, 270, and 480 kDa polypeptides. The 480-kDa peptide is the major isoform responsible for organization of the components of the axon initial segment (AIS), including the clustering of voltage-gated sodium and potassium channels important for generation of the action potential (9, 10). The 190-kDa isoform is present at dendritic spines (11,12). Many of the risk alleles for ANK3 are in the five-prime upstream region, suggestive of changes of expression (13, 14). Ankyrin-G protein expression was reduced in pyramidal AISs in superficial layers of schizophrenia cortex (15). These data suggest that ANK3 risk alleles can cause ankyrin-G loss of function.In cortex, the AISs of pyramidal n...

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“…Importantly, there may be substantial heterogeneity of premorbid intellectual functioning in BD, 62 as has been demonstrated in post-onset patients where some score lower on proxy measures of premorbid cognitive dysfunction and others do not. 5,63,64 A recent cross-diagnostic clustering study also indicated the presence of at least one subgroup comprising ~53% patients with BD and ~47% | 17 VAN RHEENEN Et Al. with SZ that demonstrated poor premorbid academic adjustment relative to controls.…”

Section: Summary and Insights Into Cognitive Trajectories From New mentioning

confidence: 99%

Current understandings of the trajectory and emerging correlates of cognitive impairment in bipolar disorder: An overview of evidence

et al. 2019

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Objectives Cognitive dysfunction affects a significant proportion of people with bipolar disorder (BD), but the cause, trajectory and correlates of such dysfunction remains unclear. Increased understanding of these factors is required to progress treatment development for this symptom dimension. Methods This paper provides a critical overview of the literature concerning the trajectories and emerging correlates of cognitive functioning in BD. It is a narrative review in which we provide a qualitative synthesis of current evidence concerning clinical, molecular, neural and lifestyle correlates of cognitive impairment in BD across the lifespan (in premorbid, prodromal, early onset, post‐onset, elderly cohorts). Results There is emerging evidence of empirical links between cognitive impairment and an increased inflammatory state, brain structural abnormalities and reduced neuroprotection in BD. However, evidence regarding the progressive nature of cognitive impairment is mixed, since consensus between different cross‐sectional data is lacking and does not align to the outcomes of the limited longitudinal studies available. Increased recognition of cognitive heterogeneity in BD may help to explain some inconsistencies in the extant literature. Conclusions Large, longitudinally focussed studies of cognition and its covariation alongside biological and lifestyle factors are required to better define cognitive trajectories in BD, and eventually pave the way for the application of a precision medicine approach for individual patients in clinical practice.

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Differences in cognitive impairment between schizophrenia and bipolar disorder: Considering the role of heterogeneity

Cited by 105 publications

References 101 publications

Retinal vascular abnormalities in schizophrenia and bipolar disorder: A window to the brain

Retinal vascular abnormalities in schizophrenia and bipolar disorder: A window to the brain

Genetic disruption of ankyrin-G in adult mouse forebrain causes cortical synapse alteration and behavior reminiscent of bipolar disorder

Current understandings of the trajectory and emerging correlates of cognitive impairment in bipolar disorder: An overview of evidence

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