Extraction of large-scale structural covariance networks from grey matter volume for Parkinson’s disease classification

AbstractBackgroundIn patients with schizophrenia, distributed abnormalities are observed in grey matter volume. A recent hypothesis posits that these distributed changes are indicative of a plastic reorganisation process occurring in response to a functional defect in neuronal information transmission. We investigated the structural covariance across various brain regions in early-stage schizophrenia to determine if indeed the observed patterns of volumetric loss conform to a coordinated pattern of structural reorganisation.MethodsStructural magnetic resonance imaging scans were obtained from 40 healthy adults and 41 age, gender and parental socioeconomic status matched patients with schizophrenia. Volumes of grey matter tissue were estimated at the regional level across 90 atlas-based parcellations. Group-level structural covariance was studied using a graph theoretical framework.ResultsPatients had distributed reduction in grey matter volume, with high degree of localised covariance (clustering) compared with controls. Patients with schizophrenia had reduced centrality of anterior cingulate and insula but increased centrality of the fusiform cortex, compared with controls. Simulating targeted removal of highly central nodes resulted in significant loss of the overall covariance patterns in patients compared with controls.ConclusionRegional volumetric deficits in schizophrenia are not a result of random, mutually independent processes. Our observations support the occurrence of a spatially interconnected reorganisation with the systematic de-escalation of conventional ‘hub’ regions. This raises the question of whether the morphological architecture in schizophrenia is primed for compensatory functions, albeit with a high risk of inefficiency.

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Dopamine Depletion Alters Macroscopic Network Dynamics in Parkinson’s Disease

10.1101/382994 ◽

2018 ◽

Author(s):

James M. Shine ◽

Peter T. Bell ◽

Elie Matar ◽

Russell A. Poldrack ◽

Simon J.G. Lewis ◽

...

Keyword(s):

Parkinson’S Disease ◽

Parkinson's Disease ◽

Large Scale ◽

Motor Symptom ◽

Grey Matter Volume ◽

Compensatory Mechanism ◽

Dopamine Depletion ◽

Network Integration ◽

Whole Brain ◽

The Impact

AbstractParkinson’s disease is primarily characterised by diminished dopaminergic function, however the impact of these impairments on large-scale brain dynamics remains unclear. It has been difficult to disentangle the direct effects of Parkinson’s disease from compensatory changes that reconfigure the functional signature of the whole brain network. To examine the causal role of dopamine depletion in network-level topology, we investigated time-varying network structure in 37 individuals with idiopathic Parkinson’s disease, both ‘On’ and ‘Off’ dopamine replacement therapy, along with 50 age-matched, healthy control subjects using resting-state functional MRI. By tracking dynamic network-level topology, we found that the Parkinson’s disease ‘Off’ state was associated with greater network-level integration than in the ‘On’ state. The extent of integration in the ‘Off’ state inversely correlated with motor symptom severity, suggesting that a shift toward a more integrated network topology may be a compensatory mechanism associated with preserved motor function in the dopamine depleted ‘Off’ state. Furthermore, we were able to demonstrate that measures of both cognitive and brain reserve (i.e., premorbid intelligence and whole brain grey matter volume) had a positive relationship with the relative increase in network integration observed in the dopaminergic ‘Off’ state. This suggests that each of these factors plays an important role in promoting network integration in the dopaminergic ‘Off’ state. Our findings provide a mechanistic basis for understanding the PD ‘Off’ state and provide a further conceptual link with network-level reconfiguration. Together, our results highlight the mechanisms responsible for pathological and compensatory change in Parkinson’s disease.

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Grey matter volume and structural covariance associated with schizotypy

Schizophrenia Research ◽

10.1016/j.schres.2020.09.021 ◽

2020 ◽

Vol 224 ◽

pp. 88-94

Author(s):

Yong-ming Wang ◽

Zhou-ya Yang ◽

Yi Wang ◽

Yan-yu Wang ◽

Xin-lu Cai ◽

...

Keyword(s):

Grey Matter ◽

Grey Matter Volume ◽

Structural Covariance ◽

Matter Volume

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The Inequality of Neural Destiny: Signatures of Life course Socioeconomic Conditions in Brain Myelination and Grey Matter Volume

10.1101/2020.06.04.20121913 ◽

2020 ◽

Author(s):

Leyla Loued-Khenissi ◽

Olga Trofimova ◽

Peter Vollenweider ◽

Pedro Marques-Vidal ◽

Martin Preisig ◽

...

Keyword(s):

Early Life ◽

Large Scale ◽

Grey Matter ◽

Grey Matter Volume ◽

Neural Function ◽

Low Ses ◽

Unique Contribution ◽

Life Conditions ◽

Matter Volume ◽

Early Life Conditions

Socioeconomic status (SES) plays a significant role in health and disease. At the same time, early-life conditions affect neural function and structure, suggesting the brain may be a conduit for the biological embedding of SES. Here, we investigate the neural signatures of SES in a large-scale population cohort aged 45–85 years. We assess both grey matter volume (GMV) and magnetization transfer (MT) saturation, indicative of myelin content. Higher SES in childhood and adulthood associated with more GMV in several brain regions, including postcentral and temporal gyri, cuneus, and cerebellum, while low SES correlated with larger entorhinal cortex volume. High childhood SES was linked to more widespread GMV differences and higher myelin content in the sensorimotor network while low SES correlated to myelin content in the temporal lobe. Crucially, childhood SES differences in adult brains persisted even after controlling for adult SES, highlighting the unique contribution of early-life conditions to neural status in older age, independent of later changes in SES. These findings inform on the biological underpinnings of social inequality, particularly as it pertains to early-life conditions.

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The relationship of symptom dimensions and grey matter volume in a transdiagnostic cohort: Results from the DFG FOR2107

10.1055/s-0039-1679161 ◽

2019 ◽

Author(s):

F Stein ◽

G Lemmer ◽

S Schmitt ◽

K Brosch ◽

E Fischer ◽

...

Keyword(s):

Grey Matter ◽

Grey Matter Volume ◽

Symptom Dimensions ◽

Matter Volume ◽

Relationship Of ◽

The Relationship

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Social cognition and brain organization in chimpanzees (Pan troglodytes) and bonobos (Pan paniscus)

10.1093/oso/9780198728511.003.0014 ◽

2018 ◽

Author(s):

William D. Hopkins ◽

Cheryl D. Stimpson ◽

Chet C. Sherwood

Keyword(s):

Social Cognition ◽

Social Behaviour ◽

Grey Matter ◽

Species Differences ◽

Pan Paniscus ◽

Grey Matter Volume ◽

Evolutionary Models ◽

Brain Organization ◽

Matter Volume ◽

Cognition Sociale

Bonobos and chimpanzees are two closely relates species of the genus Pan, yet they exhibit marked differences in anatomy, behaviour and cognition. For this reason, comparative studies on social behaviour, cognition and brain organization between these two species provide important insights into evolutionary models of human origins. This chapter summarizes studies on socio-communicative competencies and social cognition in chimpanzees and bonobos from the authors’ laboratory in comparison to previous reports. Additionally, recent data on species differences and similarities in brain organization in grey matter volume and distribution is presented. Some preliminary findings on microstructural brain organization such as neuropil space and cellular distribution in key neurotransmitters and neuropeptides involved in social behaviour and cognition is presented. Though these studies are in their infancy, the findings point to potentially important differences in brain organization that may underlie bonobo and chimpanzees’ differences in social behaviour, communication and cognition. Les bonobos et les chimpanzés sont deux espèces du genus Pan prochement liées, néanmoins ils montrent des différences anatomiques, comportementales et cognitives marquées. Pour cette raison, les études comparatives sur le comportement social, la cognition et l’organisation corticale entre ces deux espèces fournissent des idées sur les modèles évolutionnaires des origines humaines. Dans ce chapitre, nous résumons des études sur les compétences socio-communicatives et la cognition sociale chez les chimpanzés et les bonobos de notre laboratoire en comparaison avec des rapports précédents. En plus, nous présentons des données récentes sur les différences et similarités d’organisation corticale du volume et distribution de la matière grise entre espèces. Nous présentons plus de résultats préliminaires sur l’organisation corticale microstructurale comme l’espace neuropile et la division cellulaire dans des neurotransmetteurs clés et les neuropeptides impliqués dans le comportement social et la cognition. Bien que ces études sont dans leur enfance, les résultats montrent des différences d’organisation corticale importantes qui sont à la base des différences de comportement social, la communication et la cognition entre les bonobos et les chimpanzés.

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Modelling the cascade of biomarker changes in GRN-related frontotemporal dementia

Journal of Neurology Neurosurgery & Psychiatry ◽

10.1136/jnnp-2020-323541 ◽

2021 ◽

pp. jnnp-2020-323541

Author(s):

Jessica L Panman ◽

Vikram Venkatraghavan ◽

Emma L van der Ende ◽

Rebecca M E Steketee ◽

Lize C Jiskoot ◽

...

Keyword(s):

White Matter ◽

Frontotemporal Dementia ◽

Disease Severity ◽

Grey Matter ◽

Clinical Stage ◽

Data Driven ◽

Grey Matter Volume ◽

Matter Volume ◽

Mutation Carriers ◽

Individual Disease

ObjectiveProgranulin-related frontotemporal dementia (FTD-GRN) is a fast progressive disease. Modelling the cascade of multimodal biomarker changes aids in understanding the aetiology of this disease and enables monitoring of individual mutation carriers. In this cross-sectional study, we estimated the temporal cascade of biomarker changes for FTD-GRN, in a data-driven way.MethodsWe included 56 presymptomatic and 35 symptomatic GRN mutation carriers, and 35 healthy non-carriers. Selected biomarkers were neurofilament light chain (NfL), grey matter volume, white matter microstructure and cognitive domains. We used discriminative event-based modelling to infer the cascade of biomarker changes in FTD-GRN and estimated individual disease severity through cross-validation. We derived the biomarker cascades in non-fluent variant primary progressive aphasia (nfvPPA) and behavioural variant FTD (bvFTD) to understand the differences between these phenotypes.ResultsLanguage functioning and NfL were the earliest abnormal biomarkers in FTD-GRN. White matter tracts were affected before grey matter volume, and the left hemisphere degenerated before the right. Based on individual disease severities, presymptomatic carriers could be delineated from symptomatic carriers with a sensitivity of 100% and specificity of 96.1%. The estimated disease severity strongly correlated with functional severity in nfvPPA, but not in bvFTD. In addition, the biomarker cascade in bvFTD showed more uncertainty than nfvPPA.ConclusionDegeneration of axons and language deficits are indicated to be the earliest biomarkers in FTD-GRN, with bvFTD being more heterogeneous in disease progression than nfvPPA. Our data-driven model could help identify presymptomatic GRN mutation carriers at risk of conversion to the clinical stage.

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