Aberrant cerebellar neural activity and cerebro-cerebellar functional connectivity involving executive dysfunction in schizophrenia with primary negative symptoms

Gao, Ju; Tang, Xiaowei; Wang, Congjie; Yu, Miao; Sha, Wei; Wang, Xiang; Zhang, Hongying; Zhang, Xiangrong; Zhang, Xiaobin

doi:10.1007/s11682-018-0032-9

Cited by 15 publications

(11 citation statements)

References 60 publications

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“…As a result of these changes, vital neurons of the frontal cortex, hippocampus, and other regions, which are physiologically responsible for normal synaptic plasticity and neurotransmitter release are turned off [24][25][26][27]. These neurons affect learning and memory, focus, cognitive functions, and are responsible for the organization of neurons in the finely-tuned circuits and motor functions during puberty [27,28].…”

Section: Oxidative Nitrosative and Sulfuric Stress In Schizophreniamentioning

confidence: 99%

“…Those deficits, disturbing neural communication, are clinically manifested through speech and the disorders of information interpretation, auditory hallucinations, mood disorders, personality turmoil, and depression [26,27]. A decrease in brain bioelectrical activity in the inferior left crescent lobe of cerebellum may be associated with negative symptoms [28] in those patients. In addition, loss of synapses plasticity and impaired electrical conductivity can be observed, which causes elongation of the nerve impulse path and ultimately the death of neurons [29].…”

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confidence: 99%

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Oxidative-Antioxidant Imbalance and Impaired Glucose Metabolism in Schizophrenia

et al. 2020

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Schizophrenia is a neurodevelopmental disorder featuring chronic, complex neuropsychiatric features. The etiology and pathogenesis of schizophrenia are not fully understood. Oxidative-antioxidant imbalance is a potential determinant of schizophrenia. Oxidative, nitrosative, or sulfuric damage to enzymes of glycolysis and tricarboxylic acid cycle, as well as calcium transport and ATP biosynthesis might cause impaired bioenergetics function in the brain. This could explain the initial symptoms, such as the first psychotic episode and mild cognitive impairment. Another concept of the etiopathogenesis of schizophrenia is associated with impaired glucose metabolism and insulin resistance with the activation of the mTOR mitochondrial pathway, which may contribute to impaired neuronal development. Consequently, cognitive processes requiring ATP are compromised and dysfunctions in synaptic transmission lead to neuronal death, preceding changes in key brain areas. This review summarizes the role and mutual interactions of oxidative damage and impaired glucose metabolism as key factors affecting metabolic complications in schizophrenia. These observations may be a premise for novel potential therapeutic targets that will delay not only the onset of first symptoms but also the progression of schizophrenia and its complications.

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Section: Oxidative Nitrosative and Sulfuric Stress In Schizophreniamentioning

confidence: 99%

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confidence: 99%

Oxidative-Antioxidant Imbalance and Impaired Glucose Metabolism in Schizophrenia

et al. 2020

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“…FC is particularly useful in elucidating patterns of functional integration throughout the brain (i.e., how different brain regions function together) ( 36 ). Resting-state studies in schizophrenia have reported increased FC in the left orbital medial frontal cortex and right putamen regions, and reduced FC between the striatum and the right medial orbitofrontal cortex, which were significantly associated with negative symptom severity ( 37 , 38 ). These findings from functional MRI studies using ALFF, ReHo, or FC support the statement that negative symptoms are associated with aberrant activation or dysconnectivity in extensive brain regions.…”

Section: Introductionmentioning

confidence: 99%

Meta-analysis of structural and functional brain abnormalities in schizophrenia with persistent negative symptoms using activation likelihood estimation

et al. 2022

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BackgroundPersistent negative symptoms (PNS) include both primary and secondary negative symptoms that persist after adequate treatment, and represent an unmet therapeutic need. Published magnetic resonance imaging (MRI) evidence of structural and resting-state functional brain abnormalities in schizophrenia with PNS has been inconsistent. Thus, the purpose of this meta-analysis is to identify abnormalities in structural and functional brain regions in patients with PNS compared to healthy controls.MethodsWe systematically searched PubMed, Web of Science, and Embase for structural and functional imaging studies based on five research methods, including voxel-based morphometry (VBM), diffusion tensor imaging (DTI), functional connectivity (FC), the amplitude of low-frequency fluctuation or fractional amplitude of low-frequency fluctuation (ALFF/fALFF), and regional homogeneity (ReHo). Afterward, we conducted a coordinate-based meta-analysis by using the activation likelihood estimation algorithm.ResultsTwenty-five structural MRI studies and thirty-two functional MRI studies were included in the meta-analyses. Our analysis revealed the presence of structural alterations in patients with PNS in some brain regions including the bilateral insula, medial frontal gyrus, anterior cingulate gyrus, left amygdala, superior temporal gyrus, inferior frontal gyrus, cingulate gyrus and middle temporal gyrus, as well as functional differences in some brain regions including the bilateral precuneus, thalamus, left lentiform nucleus, posterior cingulate gyrus, medial frontal gyrus, and superior frontal gyrus.ConclusionOur study suggests that structural brain abnormalities are consistently located in the prefrontal, temporal, limbic and subcortical regions, and functional alterations are concentrated in the thalamo-cortical circuits and the default mode network (DMN). This study provides new insights for targeted treatment and intervention to delay further progression of negative symptoms.Systematic review registration[https://www.crd.york.ac.uk/prospero/], identifier [CRD42022338669].

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“…Between‐group differences were found in the cerebellar–cortical functional connectivity from Crus I, lobule IX, and lobule X (FDR‐corrected p < .05 with Cohen's d : .60–.65) and a trend‐level difference in Crus II ( p = .01 with Cohen's d = .50, but not surviving FDR‐correction) to the whole cortical functional networks (Figure 1 and Table S2). In the second step, we subsequently examined the connectivity of these four cerebellar lobules with the 10 cortical functional networks; Crus II was included due to the potential abnormalities found in previous schizophrenia resting‐state studies (Ding et al, 2019; Gao et al, 2019; Guo et al, 2015; Shinn et al, 2015). Our analyses revealed robust between‐group differences (FDR‐corrected p < 0.05) for the specific cortical functional networks (Figure 2 and Table S3).…”

Section: Resultsmentioning

confidence: 99%

Cerebellar–cortical dysconnectivity in resting‐state associated with sensorimotor tasks in schizophrenia

Kim

Moussa-Tooks

Bolbecker

et al. 2020

Human Brain Mapping

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Abnormalities of cerebellar function have been implicated in the pathophysiology of schizophrenia. Since the cerebellum has afferent and efferent projections to diverse brain regions, abnormalities in cerebellar lobules could affect functional connectivity with multiple functional systems in the brain. Prior studies, however, have not examined the relationship of individual cerebellar lobules with motor and nonmotor resting‐state functional networks. We evaluated these relationships using resting‐state fMRI in 30 patients with a schizophrenia‐spectrum disorder and 37 healthy comparison participants. For connectivity analyses, the cerebellum was parcellated into 18 lobular and vermal regions, and functional connectivity of each lobule to 10 major functional networks in the cerebrum was evaluated. The relationship between functional connectivity measures and behavioral performance on sensorimotor tasks (i.e., finger‐tapping and postural sway) was also examined. We found cerebellar–cortical hyperconnectivity in schizophrenia, which was predominantly associated with Crus I, Crus II, lobule IX, and lobule X. Specifically, abnormal cerebellar connectivity was found to the cerebral ventral attention, motor, and auditory networks. This cerebellar–cortical connectivity in the resting‐state was differentially associated with sensorimotor task‐based behavioral measures in schizophrenia and healthy comparison participants—that is, dissociation with motor network and association with nonmotor network in schizophrenia. These findings suggest that functional association between individual cerebellar lobules and the ventral attentional, motor, and auditory networks is particularly affected in schizophrenia. They are also consistent with dysconnectivity models of schizophrenia suggesting cerebellar contributions to a broad range of sensorimotor and cognitive operations.

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Aberrant cerebellar neural activity and cerebro-cerebellar functional connectivity involving executive dysfunction in schizophrenia with primary negative symptoms

Cited by 15 publications

References 60 publications

Oxidative-Antioxidant Imbalance and Impaired Glucose Metabolism in Schizophrenia

Oxidative-Antioxidant Imbalance and Impaired Glucose Metabolism in Schizophrenia

Meta-analysis of structural and functional brain abnormalities in schizophrenia with persistent negative symptoms using activation likelihood estimation

Cerebellar–cortical dysconnectivity in resting‐state associated with sensorimotor tasks in schizophrenia

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