White matter deficits in first episode schizophrenia: An activation likelihood estimation meta-analysis

Yao, Li; Lui, Su; Liao, Yi; Du, Mingying; Hu, Na; Thomas, Joy A.; Gong, Qiyong

doi:10.1016/j.pnpbp.2013.04.019

Cited by 137 publications

(99 citation statements)

References 92 publications

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“…Recent studies have shown that myelination is essential for social experience-based cognition and motor skill learning [31][32][33] [34][35][36] , abnormalities of the myelin sheath may contribute to defects of neuronal function. Increasing evidence has shown that the impairment of white matter integrity is prominent in schizophrenic brains [10,11,14,15] and further underscores the importance of the myelin sheath in schizophrenia, pointing to myelin repair as a potential therapeutic strategy for schizophrenia. In support of this notion, quetiapine, an atypical anti-schizophrenic drug, has been found to be potent in promoting the differentiation of OLs in vitro and enhancing remyelination in mouse models of demyelination [17][18][19][20] .…”

Section: Resultsmentioning

confidence: 99%

“…More importantly, properly myelinated nerve fibers allow precise and accurate information to fl ow within and between neuronal circuits [3,8,9] . A number of imaging studies have shown that the white matter volume of schizophrenic brains is lower than in healthy controls, suggesting that myelin sheath damage or demyelination is involved in the schizophrenic brain [10][11][12][13][14][15] . In line with this hypothesis, microarray analyses have shown that genes down-regulated in schizophrenic brains are related to OL development and myelination, arguing that myelin repair may be an unmet need that has been overlooked in therapies for schizophrenia [16] .…”

Section: Introductionmentioning

confidence: 99%

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Clemastine rescues behavioral changes and enhances remyelination in the cuprizone mouse model of demyelination

et al. 2015

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Increasing evidence suggests that white matter disorders based on myelin sheath impairment may underlie the neuropathological changes in schizophrenia. But it is unknown whether enhancing remyelination is a beneficial approach to schizophrenia. To investigate this hypothesis, we used clemastine, an FDA-approved drug with high potency in promoting oligodendroglial differentiation and myelination, on a cuprizone-induced mouse model of demyelination. The mice exposed to cuprizone (0.2% in chow) for 6 weeks displayed schizophrenia-like behavioral changes, including decreased exploration of the center in the open fi eld test and increased entries into the arms of the Y-maze, as well as evident demyelination in the cortex and corpus callosum. Clemastine treatment was initiated upon cuprizone withdrawal at 10 mg/kg per day for 3 weeks. As expected, myelin repair was greatly enhanced in the demyelinated regions with increased mature oligodendrocytes (APC-positive) and myelin basic protein. More importantly, the clemastine treatment rescued the schizophrenia-like behavioral changes in the open field test and the Y-maze compared to vehicle, suggesting a beneficial effect via promoting myelin repair. Our fi ndings indicate that enhancing remyelination may be a potential therapy for schizophrenia.

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Clemastine rescues behavioral changes and enhances remyelination in the cuprizone mouse model of demyelination

et al. 2015

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“…65 Our finding of lower FA within the IFOF among individuals higher in psychometric schizotypy is consistent with prior work implicating dysfunction of this tract in the neurobiology of SZ. For example, Yao et al 66 reported white matter deficits in first-episode SZ in the left IFOF using an activation likelihood estimation meta-analysis involving 8 studies that included 271 first-episode patients and 297 healthy controls. Moreover, the observation of lower FA within the left IFOF among first-episode neuroleptic-naive patients compared with healthy volunteers suggests these effects are not an artifact of antipsychotic medication exposure.…”

Section: Discussionmentioning

confidence: 99%

Evidence From Structural and Diffusion Tensor Imaging for Frontotemporal Deficits in Psychometric Schizotypy

DeRosse

Nitzburg

Ikuta

et al. 2014

Schizophrenia Bulletin

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Background: Previous studies of nonclinical samples exhibiting schizotypal traits have provided support for the existence of a continuous distribution of psychotic symptoms in the general population. Few studies, however, have examined the neural correlates of psychometric schizotypy using structural and diffusion tensor imaging (DTI). Methods: Healthy volunteers between the ages of 18 and 68 were recruited from the community and assessed using the Schizotypal Personality Questionnaire and received structural and DTI exams. Participants with high (N = 67) and low (N = 71) psychometric schizotypy were compared on gray and white matter volume, and cortical thickness in frontal and temporal lobe regions and on fractional anisotropy (FA) within 5 association tracts traversing the frontal and temporal lobes. Results: Higher levels of schizotypy were associated with lower overall volumes of gray matter in both the frontal and temporal lobes and lower gray matter thickness in the temporal lobe. Regionally specific effects were evident in both white matter and gray matter volume of the rostral middle frontal cortex and gray matter volume in the pars orbitalis. Moreover, relative to individuals who scored low, those who scored high in schizotypy had lower FA in the inferior fronto-occipital fasciculus as well as greater asymmetry (right > left) in the uncinate fasciculus. Conclusions: These findings are broadly consistent with recent data on the neurobiological correlates of psychometric schizotypy as well as findings in schizotypal personality disorder and schizophrenia and suggest that frontotemporal lobe dysfunction may represent a core component of the psychosis phenotype.

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“…Specifically, long-range white matter projections into the higher-order cortical regions of the frontal lobes may be associated with positive symptoms. 6,12 At a cellular level, dysfunctional glutamatergic synapses involved in synaptic plasticity may cause the delayed corollary discharges. 13 Several neurotransmitters, such as acetylcholine, serotonin and dopamine, modulate the synapses at the glutamate (N-methyl-d-aspartate [NMDA]) receptors.…”

Section: Introductionmentioning

confidence: 99%

Frontal fasciculi and psychotic symptoms in antipsychotic-naive patients with schizophrenia before and after 6 weeks of selective dopamine D2/3 receptor blockade

Ebdrup

Raghava

Nielsen

et al. 2016

jpn

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White matter deficits in first episode schizophrenia: An activation likelihood estimation meta-analysis

Cited by 137 publications

References 92 publications

Clemastine rescues behavioral changes and enhances remyelination in the cuprizone mouse model of demyelination

Clemastine rescues behavioral changes and enhances remyelination in the cuprizone mouse model of demyelination

Evidence From Structural and Diffusion Tensor Imaging for Frontotemporal Deficits in Psychometric Schizotypy

Frontal fasciculi and psychotic symptoms in antipsychotic-naive patients with schizophrenia before and after 6 weeks of selective dopamine D2/3 receptor blockade

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