Bridging disparate symptoms of schizophrenia: a triple network dysfunction theory

Nekovarova, Tereza; Fajnerová, Iveta; Horáček, Jiří; Španiel, Filip

doi:10.3389/fnbeh.2014.00171

Cited by 104 publications

(87 citation statements)

References 107 publications

(150 reference statements)

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“…In particular, the left SFG is functionally connected to most of the default mode network and suggested to play a key role in information processing between the default mode network and a number of distributed fronto-parietal control networks(54, 55). A series of studies have reported that patients with schizophrenia have exhibited distinct connectivity patterns compared to controls within(56, 57) and between(58, 59) these two networks, each tied to key domains of cognition. The superior frontal gyrus is also among the cortical territories that have vastly expanded, as a proportion of overall cortical tissue, in humans versus other primates(60).…”

Section: Discussionmentioning

confidence: 99%

Partitioning heritability analysis reveals a shared genetic basis of brain anatomy and schizophrenia

et al. 2016

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Schizophrenia is a devastating neurodevelopmental disorder with a complex genetic etiology. Widespread cortical gray matter loss has been observed in patients and prodromal samples. However, it remains unresolved whether schizophrenia-associated cortical structure variations arise due to disease etiology or secondary to the illness. Here we address this question using a partitioning-based heritability analysis of genome-wide SNP and neuroimaging data from 1,750 healthy individuals. We find that schizophrenia-associated genetic variants explain a significantly enriched proportion of trait heritability in eight brain phenotypes (FDR=10%). In particular, intracranial volume (ICV) and left superior frontal gyrus thickness exhibit significant and robust associations with schizophrenia genetic risk under varying SNP selection conditions. Cross disorder comparison suggests that the neurogenetic architecture of schizophrenia-associated brain regions is, at least in part, shared with other psychiatric disorders. Our study highlights key neuroanatomical correlates of schizophrenia genetic risk in the general population. These may provide fundamental insights into the complex pathophysiology of the illness, and a potential link to neurocognitive deficits shaping the disorder.

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Section: Discussionmentioning

confidence: 99%

Partitioning heritability analysis reveals a shared genetic basis of brain anatomy and schizophrenia

et al. 2016

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“…Psychosis and salience attribution deficits in schizophrenia are related to inter-network dysfunction between the SN, CEN and DMN (Palaniyappan et al, 2011, 2013; Moran et al, 2013; Lee et al, 2014; for a comprehensive review, see Nekovarova et al, 2014). Patients experiencing auditory hallucinations show increases in AI and frontal operculum activation and altered SN dynamics, indicating that internally generated stimuli are perceived as abnormally salient (Sommer et al, 2008; Lefebvre et al, 2016).…”

Section: Abnormalities Of Sn-cstc Loop Circuits In Psychiatric Illnessesmentioning

confidence: 99%

Cortico-Striatal-Thalamic Loop Circuits of the Salience Network: A Central Pathway in Psychiatric Disease and Treatment

Peters

Dunlop

Downar³

2016

Front. Syst. Neurosci.

430

298

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The salience network (SN) plays a central role in cognitive control by integrating sensory input to guide attention, attend to motivationally salient stimuli and recruit appropriate functional brain-behavior networks to modulate behavior. Mounting evidence suggests that disturbances in SN function underlie abnormalities in cognitive control and may be a common etiology underlying many psychiatric disorders. Such functional and anatomical abnormalities have been recently apparent in studies and meta-analyses of psychiatric illness using functional magnetic resonance imaging (fMRI) and voxel-based morphometry (VBM). Of particular importance, abnormal structure and function in major cortical nodes of the SN, the dorsal anterior cingulate cortex (dACC) and anterior insula (AI), have been observed as a common neurobiological substrate across a broad spectrum of psychiatric disorders. In addition to cortical nodes of the SN, the network’s associated subcortical structures, including the dorsal striatum, mediodorsal thalamus and dopaminergic brainstem nuclei, comprise a discrete regulatory loop circuit. The SN’s cortico-striato-thalamo-cortical loop increasingly appears to be central to mechanisms of cognitive control, as well as to a broad spectrum of psychiatric illnesses and their available treatments. Functional imbalances within the SN loop appear to impair cognitive control, and specifically may impair self-regulation of cognition, behavior and emotion, thereby leading to symptoms of psychiatric illness. Furthermore, treating such psychiatric illnesses using invasive or non-invasive brain stimulation techniques appears to modulate SN cortical-subcortical loop integrity, and these effects may be central to the therapeutic mechanisms of brain stimulation treatments in many psychiatric illnesses. Here, we review clinical and experimental evidence for abnormalities in SN cortico-striatal-thalamic loop circuits in major depression, substance use disorders (SUD), anxiety disorders, schizophrenia and eating disorders (ED). We also review emergent therapeutic evidence that novel invasive and non-invasive brain stimulation treatments may exert therapeutic effects by normalizing abnormalities in the SN loop, thereby restoring the capacity for cognitive control. Finally, we consider a series of promising directions for future investigations on the role of SN cortico-striatal-thalamic loop circuits in the pathophysiology and treatment of psychiatric disorders.

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“…attentional and self-related mental processes) 43 , and mediating the interactions between DMN and CEN 44 . The triple network model has been widely applied to illuminate the brain mechanisms of multiple disorders, including Alzheimer’s disease 45 , schizophrenia 46, 47 , depression 48 , etc. Recently, Abbott and colleagues investigated the iFC of these networks in 37 ASD and 38 typically developed (TD) participants 49 , which was the first research focusing on the three “core” neurocognitive networks in autism.…”

Section: Introductionmentioning

confidence: 99%

Altered Developmental Trajectories in Intrinsic Function between Default, Salience, and Executive Networks in High-Functioning Autism

Yang

Chen

et al. 2018

Preprint

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Although many studies have focused on abnormal patterns of brain functional connectivity in Autism spectrum disorder (ASD), one important factor, the developmental effect of brain networks was largely overlooked. To clarify the abnormal developmental trajectory of brain functional connectivity in ASD, we focused on the age-related changes in three "core" neurocognitive networks: default mode network (DMN), salience network (SN) and central executive network (CEN, also divided into left and right CEN, i.e., lCEN and rCEN). The development of intrinsic functional connectivity (iFC) within and between these networks were analyzed in 107Chinese participants, including children, adolescents, and adults (54 patients with ASD and 53 typically developed (TD) participants; ages 6-30 years). We found that diagnosis-related distinctions in age-related changes suggest three maturation patterns in networks' or nodes' iFC: delayed (iFC between SN and rCEN), ectopic (iFC between SN and DMN, and iFC between posterior cingulate cortex (PCC) and right anterior insula/dorsal anterior cingulate cortex (dACC)), and failure maturation (iFC between dACC and ventral medial prefrontal cortex). Compared with age-matched TD participants, ASD patients in children and adolescents exhibited hypo-connectivity, while that in adults showed hyper-connectivity. In addition, an independent verification based on Autism Brain Imaging Data Exchange (ABIDE) datasets confirmed our findings of developmental trajectories in ASD group, which also showed unchanged functional connectivity with age between DMN and SN and increasing iFC between rCEN and SN. The conspicuous differences in the . CC-BY-NC-ND 4.0 International license peer-reviewed) is the author/funder. It is made available under a The copyright holder for this preprint (which was not . http://dx.doi.org/10.1101/252320 doi: bioRxiv preprint first posted online Jan. 23, 2018; development of three "core" networks in ASD were demonstrated, which may lead a nuanced understanding towards the abnormal brain network maturation trajectory of autism.

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Bridging disparate symptoms of schizophrenia: a triple network dysfunction theory

Cited by 104 publications

References 107 publications

Partitioning heritability analysis reveals a shared genetic basis of brain anatomy and schizophrenia

Partitioning heritability analysis reveals a shared genetic basis of brain anatomy and schizophrenia

Cortico-Striatal-Thalamic Loop Circuits of the Salience Network: A Central Pathway in Psychiatric Disease and Treatment

Altered Developmental Trajectories in Intrinsic Function between Default, Salience, and Executive Networks in High-Functioning Autism

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