The research evidence for schizophrenia as a neurodevelopmental disorder

Rund, Bjørn Rishovd

doi:10.1111/sjop.12414

Cited by 52 publications

(36 citation statements)

References 124 publications

(173 reference statements)

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“…73 The neurodegenerative model hypothesizes that the dysfunctional development is progressive and persists after the onset of the illness, resulting in structural changes in the brain; it involves a cytopathological process with the loss of neurons and synapses and subsequent gliosis. 74 Additionally, some studies support the theory that the psychotic episode is, in itself, neurotoxic and contributes to the structural changes seen after symptom onset. 75 It appears plausible that the pathophysiology of schizophrenia could be explained by a combination of these models; it could be seen as an early neurodevelopmental aberration exacerbated by a limited ongoing neurodegenerative process, 76 recurring neurotoxic psychotic episodes, 77 or both.…”

Section: Discussionmentioning

confidence: 95%

Unconjugated bilirubin and schizophrenia: a systematic review

2019

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Schizophrenia is a complex syndrome of unknown etiology and difficult to manage. Unconjugated bilirubin has been researched as a potential biological marker of this syndrome. The objective of this review article was to gather the studies published to date on the relationship between this molecule and schizophrenia. Broad inclusion criteria have been used (PRISMA) to include as many relevant studies as possible. Fourteen studies were selected: 3 analyzed the effects of unconjugated hyperbilirubinemia in animal models; 6 demonstrated an increased incidence of schizophrenia in patients with increased unconjugated bilirubin; 2 reported an increased incidence of the disease in patients with decreased unconjugated bilirubin; and 3 linked an increased incidence of schizophrenia with an increased excretion of the oxidative product of bilirubin, the so-called biopyrrins. Because of apparently contradictory reported results, the hypothesis that the relationship between schizophrenia and unconjugated bilirubin was not linear and that there was an inflammatory dysfunction explaining this was considered. The 2 most accepted models for the pathophysiology of schizophrenia are described, and the possible role of the molecule in each is clarified. The bilirubin buffer system and its role in antioxidant defense was explored. The average levels of unconjugated bilirubin in patients with schizophrenia, schizoaffective disorder, and bipolar disorder were also compared, having been hypothesized that these diseases could be different points of a same pathological spectrum. Finally, it was concluded that unconjugated bilirubin is a promising molecule that could be used as a possible biological marker for schizophrenia, and the necessity of subsequent efforts for its research was considered.

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Section: Discussionmentioning

confidence: 95%

Unconjugated bilirubin and schizophrenia: a systematic review

2019

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“…The potential role of neurodevelopmental disorder in schizophrenia has been suggested but is still ambiguous. A recent review has detailed a pivotal role of neurodevelopmental disorder in the pathogenesis of schizophrenia (Rund, ). CACNA1C is a known marker of neurodevelopment that plays an important role in schizophrenic pathophysiology (Bhat et al, ; Blake et al, ; Yin et al, ).…”

Section: Discussionmentioning

confidence: 99%

CACNA1C (rs1006737) may be a susceptibility gene for schizophrenia: An updated meta‐analysis

et al. 2019

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Introduction Schizophrenia is a serious mental illness with a genetic predisposition. Genome‐wide association studies (GWAS) have identified the α‐1C subunit of the L‐type voltage‐gated calcium channel ( CACNA1C ) gene as a significant risk gene for schizophrenia. However, there are inconsistent conclusions in case–control studies. Methods We performed a comprehensive meta‐analysis of all available samples from existing studies under four different genetic models (recessive model, dominant model, additive model and allele model) to further confirm whether CACNA1C rs1006737 is an authentic risk single nucleotide polymorphism (SNP) for schizophrenia. Results A statistically significant difference under the four models (all p < 0.05) was observed by pooling nine Asian and European studies, including a total of 12,744 cases and 16,460 controls. For European‐decent samples, a significant difference was identified between patients and controls for the four models (all p < 0.05). We observed a significant difference between patients and controls for the recessive model and allele model (GG vs. GA + AA: p < 0.00001; G vs. A: p < 0.00001) using a fixed effect model, but the dominant model (GG + GA vs. AA: OR: p = 0.15) and additive model (GG vs. AA: p = 0.11) showed no significant difference between patients and controls in the Asian samples. Conclusion Our findings provide important evidence for the establishment of CACNA1C as a susceptibility gene for schizophrenia across world populations, but its roles in the pathogenesis of schizophrenia need to be further investigated.

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“…The main debate regarding the cognitive course in schizophrenia is about whether it follows a neurodevelopmental or neurodegenerative course , Rund, 2018.…”

Section: The Cognitive Course In Schizophreniamentioning

confidence: 99%

The relationship between level of cognitive impairments and functional outcome trajectories in first-episode schizophrenia

Czajkowski

Rund

et al. 2017

Schizophrenia Research

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Although cognitive impairments are consistently linked to functional outcome in chronic schizophrenia, the relationship remains unclear for patients with first-episode schizophrenia. The objective of this present study was to determine whether there are distinct developmental trajectories for functional outcome in patients with different levels of baseline cognition. The present study has a multi-follow-up design, and includes data from six follow-ups over four years. Assessments were conducted yearly, apart from the first year where assessments were conducted every six months. A total of 28 patients with first-episode schizophrenia participated in the study, with 79% of patients retained at the 4-year follow-up. Cognition was assessed with MATRICS Consensus Cognitive Battery. Functional outcomes were obtained through Global functioning: Social and Global functioning: Role. Data were analyzed with linear multilevel models. Results suggest steady improvements in social and role functioning among the patients across the four year period. Baseline attention, verbal learning, and verbal working memory were significantly associated with social outcome. Role functioning was significantly associated with attention, verbal working memory, and reasoning/problem solving. Furthermore, the rate of change in social outcome varies among patients depending on their baseline level of attention and verbal working memory, with the lowest scoring group showing the least improvement over the years. The subgroup of patients with the largest cognitive impairments at the onset of the disorder shows limited improvements in social functioning compared to higher functioning groups.

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The research evidence for schizophrenia as a neurodevelopmental disorder

Cited by 52 publications

References 124 publications

Unconjugated bilirubin and schizophrenia: a systematic review

Unconjugated bilirubin and schizophrenia: a systematic review

CACNA1C (rs1006737) may be a susceptibility gene for schizophrenia: An updated meta‐analysis

The relationship between level of cognitive impairments and functional outcome trajectories in first-episode schizophrenia

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