The neurobiology of transition to psychosis

Palaniyappan, Lena; Das, Tushar Kanti; Dempster, Kara

doi:10.1503/jpn.170137

Cited by 14 publications

(11 citation statements)

References 108 publications

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“…Furthermore, the same authors showed that resilient UHR individuals have increased volume and surface area compared with non-resilient UHR and to controls, suggesting the presence of compensatory neural mechanisms that may prevent a worse outcome. This hypothesis was further supported by Palaniyappan et al (2017). Therefore, we can speculate that our results could be driven by the resilient UHR individuals with 22q11DS.…”

Section: Discussionsupporting

confidence: 62%

“…We further showed a predominant increase in cortical volume and surface area in patients with 22q11DS fulfilling UHR criteria. While initial investigations conducted in non-deleted UHR individuals mainly pointed to reduced grey matter, recent investigations reported contradictory results, suggesting the presence of higher grey matter volume in UHR individuals (Schaufelberger et al 2011; de Wit et al 2016; Dukart et al 2017; Palaniyappan et al 2017). For instance, Dukart et al .…”

Section: Discussionmentioning

confidence: 99%

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Cortical morphology development in patients with 22q11.2 deletion syndrome at ultra-high risk of psychosis

et al. 2018

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Section: Discussionsupporting

confidence: 62%

Section: Discussionmentioning

confidence: 99%

Cortical morphology development in patients with 22q11.2 deletion syndrome at ultra-high risk of psychosis

et al. 2018

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“…Therefore, we suggest that increased CSA in UHR subjects might reflect aberrant or delayed pruning. It is also conceivable, that increased CSA occurs due to insufficient (or delayed) intracortical myelination 60 . Reduced myelination in schizophrenic patients support this suggestion 61 , as well as post-mortem and genomic studies, summarized in Palaniyappan et al 60 .…”

Section: Discussionmentioning

confidence: 99%

Cortical Volume Differences in Subjects at Risk for Psychosis Are Driven by Surface Area

Buechler

Wotruba

Michels

et al. 2020

Schizophrenia Bulletin

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In subjects at risk for psychosis, the studies on gray matter volume (GMV) predominantly reported volume loss compared with healthy controls (CON). However, other important morphological measurements such as cortical surface area (CSA) and cortical thickness (CT) were not systematically compared. So far, samples mostly comprised subjects at genetic risk or at clinical risk fulfilling an ultra-high risk (UHR) criterion. No studies comparing UHR subjects with at-risk subjects showing only basic symptoms (BS) investigated the differences in CSA or CT. Therefore, we aimed to unravel the contribution of the 2 morphometrical measures constituting the cortical volume (CV) and to test whether these groups inhere different morphometric features. We conducted a surface-based morphometric analysis in 34 CON, 46 BS, and 39 UHR to examine between-group differences in CV, CSA, and CT vertex-wise across the whole cortex. Compared with BS and CON, UHR individuals presented increased CV in frontal and parietal regions, which was driven by larger CSA. These groups did not differ in CT. Yet, at-risk subjects who later developed schizophrenia showed thinning in the occipital cortex. Furthermore, BS presented increased CSA compared with CON. Our results suggest that volumetric differences in UHR subjects are driven by CSA while CV loss in converters seems to be based on cortical thinning. We attribute the larger CSA in UHR to aberrant pruning representing a vulnerability to develop psychotic symptoms reflected in different levels of vulnerability for BS and UHR, and cortical thinning to a presumably stress-related cortical decomposition.

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“…A number of myelin gene knockout mice models exhibit schizophrenia-like behaviours, while genomic, especially GWAS, studies identified new schizophre-nia loci related to oligodendrocyte genetic polymorphisms. Palaniyappan et al 80 pointed the need to revise our current "deficit-oriented" models of neurobiology of psychosis to the concept of a dynamic process of cortical reorganization, suggesting that early deficits are temporally restricted to the first few years but ameliorate with time, probably owing to a reorganization process. Future studies that employ additional dMRI-techniques for white matter microstructural assessment could better characterize the neurobiological processes that underlie macro-scale connectivity alterations across psychosis stages.…”

Section: Resultsmentioning

confidence: 99%

Is psychosis a dysmyelination-related information-processing disorder?

Giotakos¹

2019

Psychiatriki

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N umerous lines of evidence implicate myelin and oligodendrocyte function as critical processes affecting neuronal connectivity, which is a central abnormality in schizophrenia. Neurodevelopmental models related to dysmyelination have suggested its relation with different schizophrenia-like symptoms. Post-mortem studies in patients with schizophrenia have reported 14-22% reduction in the density and the quantity of oligodendrocytes. Several myelin-related candidate genes have been linked oligodendrocyte and myelin dysfunction with neurocircuitry abnormalities in schizophrenia. A number of myelin gene knockout mice models exhibit schizophrenia-like behaviours, and genomic, especially GWAS, studies identified new schizophrenia loci related to oligodendrocyte genetic polymorphisms. It is known that myelin acts as electrical insulation for the ensheathed axon, which helps to preserve the amplitude and to increase the conduction velocity of the propagating axon potential. A growing body of evidence points towards the involvement of dysmyelination of the prefrontal cortex in the development of the cognitive symptoms of psychosis. Neuroimaging investigations have linked processing speed to brain anatomical connectivity, and have pointed the role of processing speed among the predictors of clinical changes in schizophrenia. The dysmyelination-induced delays in patients with psychosis may cause a discrepancy in sensory feedback mechanisms, which results in prediction error. The myelin abnormalities and the resulting conduction delays vary during the course of the multiple sclerosis and this type of cycles are possibly associated with fluctuations in conduction velocity in psychosis. It is worthy of note that the major histocompatibility complex (MHC) is responsible for the genetic overlap in both multiple sclerosis and schizophrenia. Multiple sclerosis manifests sensory and motor symptoms, and schizophrenia disordered cognition and emotion. Having in mind the interdependent relationship of oligodendrocytes and the axons they myelinate, we could suggest that both multiple sclerosis and schizophrenia may use in central nervous system a common pathway of disordered information-processing. Recent research suggests that adaptive myelination could normalize neuronal electrical excitability, which in turn can modify myelin plasticity, resulting to neural activity and behavior modulation. We may suggest that interventions that preserve white matter integrity or ameliorate white matter disruption may enhance information-processing and functional outcome in psychosis.

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The neurobiology of transition to psychosis

Cited by 14 publications

References 108 publications

Cortical morphology development in patients with 22q11.2 deletion syndrome at ultra-high risk of psychosis

Cortical morphology development in patients with 22q11.2 deletion syndrome at ultra-high risk of psychosis

Cortical Volume Differences in Subjects at Risk for Psychosis Are Driven by Surface Area

Is psychosis a dysmyelination-related information-processing disorder?

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