Regional cortical thinning in young adults with schizophrenia but not psychotic or non-psychotic bipolar I disorder

Godwin, Douglass; Alpert, Kathryn I.; Wang, Lei; Mamah, Daniel

doi:10.1186/s40345-018-0124-x

Cited by 19 publications

(9 citation statements)

References 92 publications

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“…Previous studies have found anhedonia to be associated with reduced volume or CT in these regions within non-clinical populations (14, 15), as well as in patients with schizophrenia and MDD (10, 31-33). In addition, we found a negative association between state anhedonia and CT in the paracentral cortex and pars opercularis, consistent with previous studies in patients with schizophrenia (9, 10, 34, 35), corresponding to their potential roles in reward anticipation to some extent (36, 37). Neuroanatomical alterations in these reward-related brain regions may lead to functional deficits in motivation and goal-directed behavior, thereby giving rise to loss of the capacity to experience pleasure.…”

Section: Discussionsupporting

confidence: 92%

Phenotypic and genetic associations between anhedonia and brain structure in UK Biobank

Cullen

Lyall

Strawbridge

et al. 2020

Preprint

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Background: Anhedonia is a core symptom of multiple psychiatric disorders and has been associated with changes in brain structure. Genome-wide association studies suggest that anhedonia is heritable with a polygenic architecture but few studies have explored the association between genetic loading for anhedonia - indexed by polygenic risk scores for anhedonia (PRS-anhedonia) - and structural brain imaging phenotypes. We investigated how anhedonia and polygenic risk for anhedonia were associated with brain structure within the UK Biobank cohort. Methods: Brain measures (including total grey/white matter volumes, subcortical volumes, cortical thickness and white matter integrity) were analysed in relation to the self-reported anhedonia phenotype and PRS-anhedonia for 17,492 participants (8,506 males and 8,986 females; mean age = 62.81 years, SD = 7.43), using linear mixed models and including mediation analyses. Results: State anhedonia was significantly associated with smaller total grey matter volume (GMV), smaller volumes in thalamus and nucleus accumbens; as well as reduced cortical thickness within the paracentral gyrus, the opercular part of inferior frontal gyrus and the rostral anterior cingulate cortex. PRS-anhedonia was associated with reduced total GMV, increased total white matter volume and reduced white matter integrity; in addition to reduced cortical thickness within the parahippocampal cortex, the superior temporal gyrus and the insula cortex. Conclusions: Both the state anhedonia phenotype and PRS-anhedonia were associated with differences in multiple brain structures/areas, including within reward-related circuits. These differences may represent vulnerability markers for psychopathology across a range of psychiatric disorders.

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Section: Discussionsupporting

confidence: 92%

Phenotypic and genetic associations between anhedonia and brain structure in UK Biobank

Cullen

Lyall

Strawbridge

et al. 2020

Preprint

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“…Frangou, Doucett, Lee, and Sprooten () found higher intracortical myelin concentration in the parietal cortex in SZ. Godwin and colleagues found cortical thickness was reduced in IPL and SMG in SZ (Godwin, Alpert, Wang, & Mamah, ). Cortical thinning is related to higher cortical myelin content in superficial cortical layer of IPL and SMG (Shafee et al, ), suggesting that our results were consistent with these previous studies.…”

Section: Discussionmentioning

confidence: 99%

Depth‐dependent abnormal cortical myelination in first‐episode treatment‐naïve schizophrenia

Wei

Zhang

et al. 2020

Human Brain Mapping

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Myelination is key to effective message passing in the central nervous system and is likely linked to the pathogenesis of schizophrenia (SZ). Emerging evidence indicates that a large portion of intracortical myelin insulates inhibitory interneurons that are highly relevant to pathogenesis of schizophrenia. Here for the first time, we characterized intracortical myelination across the entire cortical surface in first‐episode treatment‐naïve patients with schizophrenia (FES) using T1w/T2w ratio of structural MRI, FES patients exhibited significantly higher myelin content in the left inferior parietal lobe, supramarginal gyrus, and superior temporal gyrus in the superficial layer, as well as left IPL in the middle layer, but significantly lower myelin content in the left middle insula and posterior cingulate gyrus. Years of education, a proxy for onset of functional decline, significantly altered the relationship between abnormal parietal and posterior cingulate myelination and clinical symptoms, indicating that the pathoplastic role of myelination hinges on the age of onset of functional decline. In addition, higher myelination generally related to better cognitive function in younger subjects but worse cognitive function in older subjects. We conclude that FES is characterized by increased myelination of the superficial layers of the parietal–temporal association cortex, but reduced myelination of the cingulo‐insular midcortical layer cortex. Intracortical myelin content affects both cognitive functioning and symptom burden in FES, with the effect conditional upon age and timing of onset of functional decline. These results suggest myelination might be a critical biological target for procognitive interventions in SZ.

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“…While seemingly relatively stable and not linked to the duration of illness 20 , 21 , these morphological abnormalities have been linked to symptomology albeit inconsistently. Associations between positive symptom severity and thinning in frontal and temporal regions have been identified in SZH 22 , 23 and first episode patients 21 ; associations with negative symptoms seem less reliable. Abnormalities also link to the degree of cognitive impairment.…”

Section: Introductionmentioning

confidence: 95%

Cognitive impairment in schizophrenia: relationships with cortical thickness in fronto-temporal regions, and dissociability from symptom severity

2021

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Cognitive impairments are a core and persistent characteristic of schizophrenia with implications for daily functioning. These show only limited response to antipsychotic treatment and their neural basis is not well characterised. Previous studies point to relationships between cortical thickness and cognitive performance in fronto-temporal brain regions in schizophrenia patients (SZH). There is also evidence that these relationships might be independent of symptom severity, suggesting dissociable disease processes. We set out to explore these possibilities in a sample of 70 SZH and 72 age and gender-matched healthy controls (provided by the Center of Biomedical Research Excellence (COBRE)). Cortical thickness within fronto-temporal regions implicated by previous work was considered in relation to performance across various cognitive domains (from the MATRICS Cognitive Battery). Compared to controls, SZH had thinner cortices across most fronto-temporal regions and significantly lower performance on all cognitive domains. Robust relationships with cortical thickness were found: visual learning and attention performance correlated with bilateral superior and middle frontal thickness in SZH only. Correlations between attention performance and right transverse temporal thickness were also specific to SZH. Findings point to the importance of these regions for cognitive performance in SZH, possibly reflecting compensatory processes and/or aberrant connectivity. No links to symptom severity were observed in these regions, suggesting these relationships are dissociable from underlying psychotic symptomology. Findings enhance understanding of the brain structural underpinnings and possible aetiology of cognitive impairment in SZH.

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Regional cortical thinning in young adults with schizophrenia but not psychotic or non-psychotic bipolar I disorder

Cited by 19 publications

References 92 publications

Phenotypic and genetic associations between anhedonia and brain structure in UK Biobank

Phenotypic and genetic associations between anhedonia and brain structure in UK Biobank

Depth‐dependent abnormal cortical myelination in first‐episode treatment‐naïve schizophrenia

Cognitive impairment in schizophrenia: relationships with cortical thickness in fronto-temporal regions, and dissociability from symptom severity

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