The neuropathology of schizophrenia: A selective review of past studies and emerging themes in brain structure and cytoarchitecture

Bakhshi, Kirran; Chance, Steven A.

doi:10.1016/j.neuroscience.2015.06.028

Cited by 112 publications

(84 citation statements)

References 241 publications

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“…The results are congruent with multiple postmortem and imaging data that consistently show no major brain pathology in patients with psychoses [52,53,54]. Still, future studies should attempt to identify more subtle neuronal deficiencies likely present in Nrg3 KO mice as it has been demonstrated in various Nrg1 and Erb4 genetic murine models [55,56].…”

Section: Discussionsupporting

confidence: 82%

Neuregulin 3 Knockout Mice Exhibit Behaviors Consistent with Psychotic Disorders

Hayes

Shevëlkin

Zeledon³

et al. 2016

Complex Psychiatry

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Neuregulin 3 (NRG3) is a paralog of NRG1. Genetic studies in schizophrenia demonstrate that risk variants in NRG3 are associated with cognitive and psychotic symptom severity, and several intronic single nucleotide polymorphisms in NRG3 are associated with delusions in patients with schizophrenia. In order to gain insights into the biological function of the gene, we generated a novel Nrg3 knockout (KO) mouse model and tested for neurobehavioral phenotypes relevant to psychotic disorders. KO mice displayed novelty-induced hyperactivity, impaired prepulse inhibition of the acoustic startle response, and deficient fear conditioning. No gross cytoarchitectonic or layer abnormalities were noted in the brain of KO mice. Our findings suggest that deletion of the Nrg3 gene leads to alterations consistent with aspects of schizophrenia. We propose that KO mice will provide a valuable animal model to determine the role of the NRG3 in the molecular pathogenesis of schizophrenia and other psychotic disorders.

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Section: Discussionsupporting

confidence: 82%

Neuregulin 3 Knockout Mice Exhibit Behaviors Consistent with Psychotic Disorders

Hayes

Shevëlkin

Zeledon³

et al. 2016

Complex Psychiatry

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“…Usually, people with schizophrenia exhibit language problems at all levels, from phonology to pragmatics, which coalesce into problems for speech perception (auditory verbal hallucinations), abnormal speech production (formal thought disorder), and production of abnormal linguistic content (delusions, commonly understood to be distinct from thought disorders), which are the hallmarks of the disease in the domain of language (Stephane et al, 2007, 2014; Bakhshi and Chance, 2015). Importantly, although schizophrenia is commonly defined as a disturbance of thought or selfhood, some authors claim that most of its distinctive symptoms may arise from language dysfunction; in particular, from failures in language-mediated forms of meaning (Hinzen and Rosselló, 2015).…”

Section: Introductionmentioning

confidence: 99%

Bridging the Gap between Genes and Language Deficits in Schizophrenia: An Oscillopathic Approach

Murphy

Benítez‐Burraco

2016

Front. Hum. Neurosci.

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Schizophrenia is characterized by marked language deficits, but it is not clear how these deficits arise from the alteration of genes related to the disease. The goal of this paper is to aid the bridging of the gap between genes and schizophrenia and, ultimately, give support to the view that the abnormal presentation of language in this condition is heavily rooted in the evolutionary processes that brought about modern language. To that end we will focus on how the schizophrenic brain processes language and, particularly, on its distinctive oscillatory profile during language processing. Additionally, we will show that candidate genes for schizophrenia are overrepresented among the set of genes that are believed to be important for the evolution of the human faculty of language. These genes crucially include (and are related to) genes involved in brain rhythmicity. We will claim that this translational effort and the links we uncover may help develop an understanding of language evolution, along with the etiology of schizophrenia, its clinical/linguistic profile, and its high prevalence among modern populations.

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“…Comprehensive review of post-mortem studies suggests that the major contributor to GM volumetric loss in schizophrenia is synaptic regression involving glutamatergic excitatory synapses 110,222 . On the other hand, functional deficits related to reduced levels of GAD67 enzyme, rather than actual loss of parvalbumin containing interneurons, are now wellestablished in patients with schizophrenia 223 .…”

Section: Gaba and Glutamate Systemmentioning

confidence: 99%

Inefficient Neural Self-Stabilization: A theory of spontaneous resolutions and recurrent relapses in psychosis

Palaniyappan

2018

Preprint

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The neuropathology of schizophrenia: A selective review of past studies and emerging themes in brain structure and cytoarchitecture

Cited by 112 publications

References 241 publications

Neuregulin 3 Knockout Mice Exhibit Behaviors Consistent with Psychotic Disorders

Neuregulin 3 Knockout Mice Exhibit Behaviors Consistent with Psychotic Disorders

Bridging the Gap between Genes and Language Deficits in Schizophrenia: An Oscillopathic Approach

Inefficient Neural Self-Stabilization: A theory of spontaneous resolutions and recurrent relapses in psychosis

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