ORCID Profile
0000-0002-6715-1060
Current Organisation
Deakin University
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Publisher: SAGE Publications
Date: 28-02-2012
Abstract: In this article, the ontology, epistemology and methodology of anthropology are questioned with the purpose of arguing for the possibility of a neuroanthropological approach capable of investigating the relationships between the neural, the experiential and the cultural. The author contends that the dichotomization of objects and subjects, objectivism and subjectivism, and explanation and understanding that characterizes anthropology is no longer viable and that a dialectical alternative is required that regards each member of these dyads as standing in a dependent relationship to one another. It is shown that this dialectical view ultimately calls for the investigation of the neural and mental dimensions of human activity as they are embedded in their cultural matrix. The discussion is substantiated by reference to debates around how to bridge the gap between the mental and the neural. The author draws on his experience in anthropology and imaging neuroscience to assess the process of knowledge generation in both fields with a view to showing that science and humanism are interdependent. Following from this, neuroanthropology, and anthropology more broadly, are characterized as having to oscillate between scientific humanism and humanistic scientism.
Publisher: Elsevier BV
Date: 02-2020
Publisher: Elsevier BV
Date: 02-2015
DOI: 10.1016/J.BIOSYSTEMS.2014.12.003
Abstract: Degeneracy is a word with two meanings. The popular usage of the word denotes deviance and decay. In scientific discourse, degeneracy refers to the idea that different pathways can lead to the same output. In the biological sciences, the concept of degeneracy has been ignored for a few key reasons. Firstly, the word "degenerate" in popular culture has negative, emotionally powerful associations that do not inspire scientists to consider its technical meaning. Secondly, the tendency of searching for single causes of natural and social phenomena means that scientists can overlook the multi-stranded relationships between cause and effect. Thirdly, degeneracy and redundancy are often confused with each other. Degeneracy refers to dissimilar structures that are functionally similar while redundancy refers to identical structures. Degeneracy can give rise to novelty in ways that redundancy cannot. From genetic codes to immunology, vaccinology and brain development, degeneracy is a crucial part of how complex systems maintain their functional integrity. This review article discusses how the scientific concept of degeneracy was imported into genetics from physics and was later introduced to immunology and neuroscience. Using ex les of degeneracy in immunology, neuroscience and linguistics, we demonstrate that degeneracy is a useful way of understanding how complex systems function. Reviewing the history and theoretical scope of degeneracy allows its usefulness to be better appreciated, its coherency to be further developed, and its application to be more quickly realized.
Publisher: Royal College of Psychiatrists
Date: 06-2016
DOI: 10.1192/BJP.BP.114.156588
Abstract: The discovery of potential disease-modifying therapies in a neurodegenerative condition like Huntington's disease depends on the availability of sensitive biomarkers that reflect decline across disease stages and that are functionally and clinically relevant. To quantify macrostructural and microstructural changes in participants with premanifest and symptomatic Huntington's disease over 30 months, and to establish their functional and clinical relevance. Multimodal magnetic resonance imaging study measuring changes in macrostructural (volume) and microstructural (diffusivity) measures in 40 patients with premanifest Huntington's disease, 36 patients with symptomatic Huntington's disease and 36 healthy control participants over three testing sessions spanning 30 months. Relative to controls, there was greater longitudinal atrophy in participants with symptomatic Huntington's disease in whole brain, grey matter, caudate and putamen, as well as increased caudate fractional anisotropy caudate volume loss was the only measure to differ between premanifest Huntington's disease and control groups. Changes in caudate volume and fractional anisotropy correlated with each other and neurocognitive decline caudate volume loss also correlated with clinical and disease severity. Caudate neurodegeneration, especially atrophy, may be the most suitable candidate surrogate biomarker for consideration in the development of upcoming clinical trials.
Publisher: Oxford University Press (OUP)
Date: 04-08-2009
DOI: 10.1093/SCAN/NSP024
Publisher: Frontiers Media SA
Date: 22-09-2015
Publisher: MIT Press
Date: 2023
DOI: 10.1162/NETN_A_00277
Abstract: Graph theoretical analysis of the structural connectome has been employed successfully to characterize brain network alterations in patients with traumatic brain injury (TBI). However, heterogeneity in neuropathology is a well-known issue in the TBI population, such that group comparisons of patients against controls are confounded by within-group variability. Recently, novel single-subject profiling approaches have been developed to capture inter-patient heterogeneity. We present a personalized connectomics approach that examines structural brain alterations in five chronic patients with moderate to severe TBI who underwent anatomical and diffusion magnetic resonance imaging. We generated in idualized profiles of lesion characteristics and network measures (including personalized graph metric GraphMe plots, and nodal and edge-based brain network alterations) and compared them against healthy reference cases (N = 12) to assess brain damage qualitatively and quantitatively at the in idual level. Our findings revealed alterations of brain networks with high variability between patients. With validation and comparison to stratified, normative healthy control comparison cohorts, this approach could be used by clinicians to formulate a neuroscience-guided integrative rehabilitation program for TBI patients, and for designing personalized rehabilitation protocols based on their unique lesion load and connectome.
Publisher: Elsevier BV
Date: 05-2016
DOI: 10.1016/J.JNS.2016.03.021
Abstract: Subjective reports of sleep disturbance are a common feature of Huntington's disease (HD) however, there is limited research investigating the relationship between sleep problems with changes in brain and behaviour. This study aimed to investigate whether subjective reports of sleep problems in HD are associated with brain volume, neurocognitive decline, and neuropsychiatric symptoms. This retrospective pilot study used brain volume, neurocognitive and neuropsychiatric data from premanifest (pre-HD) and symptomatic HD (symp-HD). Subjective sleep problem was measured using the sleep item of the Beck's Depression Inventory-II (BDI-II). Pre-HD in iduals reporting sleep problems had significantly poorer neuropsychiatric outcomes compared to those not reporting sleep problems. In the symp-HD group, those with sleep problems had significantly accelerated thalamic degeneration and poorer neuropsychiatric outcomes compared to those without sleep problems. There was no relationship between subjective sleep problems and neurocognitive measures. These findings suggest an association between subjective sleep disturbance, neuropathology, and development of neuropsychiatric symptoms in HD. Further studies using quantitative EEG-based monitoring of sleep in HD and changes in the brain and behaviour will be necessary to establish the causal nature of this relationship.
Publisher: Elsevier BV
Date: 03-2013
DOI: 10.1016/J.NBD.2012.10.001
Abstract: We investigated two measures of neural integrity, T1-weighted volumetric measures and diffusion tensor imaging (DTI), and explored their combined potential to differentiate pre-diagnosis Huntington's disease (pre-HD) in iduals from healthy controls. We applied quadratic discriminant analysis (QDA) to discriminate pre-HD in iduals from controls and we utilised feature selection and dimension reduction to increase the robustness of the discrimination method. Thirty six symptomatic HD (symp-HD), 35 pre-HD, and 36 control in iduals participated as part of the IMAGE-HD study and underwent T1-weighted MRI, and DTI using a Siemens 3 Tesla scanner. Volume and DTI measures [mean diffusivity (MD) and fractional anisotropy (FA)] were calculated for each group within five regions of interest (ROI caudate, putamen, pallidum, accumbens and thalamus). QDA was then performed in a stepwise manner to differentiate pre-HD in iduals from controls, based initially on unimodal analysis of motor or neurocognitive measures, or on volume, MD or FA measures from within the caudate, pallidum and putamen. We then tested for potential improvements to this model, by examining multi-modal MRI classifications (volume, FA and MD), and also included motor and neurocognitive measures, and additional brain regions (i.e., accumbens and thalamus). Volume, MD and FA differed across the three groups, with pre-HD characterised by significant volumetric reductions and increased FA within caudate, putamen and pallidum, relative to controls. The QDA results demonstrated that the differentiation of pre-HD from controls was highly accurate when both volumetric and diffusion data sets from basal ganglia (BG) regions were used. The highest discriminative accuracy however was achieved in a multi-modality approach and when including all available measures: motor and neurocognitive scores and multi-modal MRI measures from the BG, accumbens and thalamus. Our QDA findings provide evidence that combined multi-modal imaging measures can accurately classify in iduals up to 15 years prior to onset when therapeutic intervention is likely to have maximal effects in slowing the trajectory of disease development.
Publisher: Informa UK Limited
Date: 03-04-2018
Publisher: Public Library of Science (PLoS)
Date: 16-09-2013
Publisher: Center for Open Science
Date: 03-12-2020
Abstract: The human brain is a dynamic network comprised of elements which are structurally connected and functionally interactive. A tight structure-function relationship is vital for this system to produce seamless cognition and behaviour. Brain injuries due to either neurological disease or single-event injuries alter the dynamics of normal structure-function interaction, resulting in poor neurobehavioural outcomes for patients. This scoping review is a synthesis of recent progress in understanding how brain injuries alter the structure-function relationship. We identified 16 studies that investigated the structure-function relationship in brain-injured cohorts, using fMRI and either T1-weighted or diffusion-weighted MRI to calculate, respectively, grey matter density or structural connectivity. Overall, a reduced structure-function relationship was found in brain-injured patients relative to healthy controls. This weakened relationship coincided with impaired cognition. Structural and functional MRI information should also be reconciled into suitable graph theoretical frameworks such as the multilayer network approach
Publisher: Elsevier BV
Date: 2020
DOI: 10.1016/J.JNS.2019.116522
Abstract: Hypothalamic pathology is a well-documented feature of Huntington's disease (HD) and is believed to contribute to circadian rhythm and habitual sleep disturbances. Currently, no therapies exist to combat hypothalamic changes, nor circadian rhythm and habitual sleep disturbances in HD. To evaluate the effects of multidisciplinary rehabilitation on hypothalamic volume, brain-derived neurotrophic factor (BDNF), circadian rhythm and habitual sleep in in iduals with preclinical HD. Eighteen in iduals with HD (ten premanifest and eight prodromal) undertook a nine-month multidisciplinary rehabilitation intervention (intervention group), which included exercise, cognitive and dual task training and social events, and were compared to a community s le of eleven in iduals with premanifest HD receiving no intervention (control group). Hypothalamic volume, serum BDNF, salivary cortisol and melatonin concentrations, subjective sleep quality, daytime somnolence, habitual sleep-wake patterns, stress and anxiety and depression symptomatology were evaluated. Hypothalamus grey matter volume loss was significantly attenuated in the intervention group compared to the control group after controlling for age, gender, Unified Huntington's Disease Rating Scale-Total Motor Score and number of cytosine-adenine-guanine repeats. Serum BDNF levels were maintained in the intervention group, but decreased in the control group following the study period. Both groups exhibited decreases in cortisol and melatonin concentrations. No changes were observed in sleep or mood outcomes. This exploratory study provides evidence that multidisciplinary rehabilitation can reduce hypothalamic volume loss and maintain peripheral BDNF levels in in iduals with preclinical HD but may not impact on circadian rhythm. Larger, randomised controlled trials are required to confirm these findings.
Publisher: Informa UK Limited
Date: 26-10-2018
DOI: 10.1080/17470919.2017.1392342
Abstract: The role of the orbitofrontal cortex (OFC) in moral decision-making is well established. However, OFC activity is highly context dependent. It is affected by the extent to which choices are morally justified and whom they concern. In the current study, we specifically focus on contextual factors and investigate the differential role of the OFC during justified and unjustified violence towards ingroup versus outgroup members. Muslims were chosen as the outgroup, as they are currently stereotypically seen as an outgroup and a potential threat by some Non-Muslims. Importantly, we also introduce a context where participants are the actual agents responsible for doing harm. During fMRI scanning, Non-Muslim participants had to decide to either shoot a Non-Muslim (i.e., ingroup member) or Muslim (outgroup member) depending on whether they believed the target was holding a gun or an object. Neuroimaging results showed increased activation in the lateral OFC (lOFC) in the three contrasts that were distressing: 1) during unjustifiable killing 2) when being killed and 3) when confronted by an outgroup member with a gun. Together, these results provide important insights into the neurocognitive mechanisms involved in intergroup violence and highlight the critical role of the lOFC in context dependent social decision-making.
Publisher: Wiley
Date: 06-06-2021
DOI: 10.1111/PSYP.13871
Abstract: Attentional lapses interfere with goal‐directed behaviors, which may result in harmless (e.g., not hearing instructions) or severe (e.g., fatal car accident) consequences. Task‐related functional MRI (fMRI) studies have shown a link between attentional lapses and activity in the frontoparietal network. Activity in this network is likely to be mediated by the organization of the white matter fiber pathways that connect the regions implicated in the network, such as the superior longitudinal fasciculus I (SLF‐I). In the present study, we investigate the relationship between susceptibility to attentional lapses and relevant white matter pathways in 36 healthy adults (23 females, M age = 31.56 years). Participants underwent a diffusion MRI (dMRI) scan and completed the global–local task to measure attentional lapses, similar to previous fMRI studies. Applying the fixel‐based analysis framework for fiber‐ specific analysis of dMRI data, we investigated the association between attentional lapses and variability in microstructural fiber density (FD) and macrostructural (morphological) fiber‐bundle cross section (FC) in the SLF‐I. Our results revealed a significant negative association between higher total number of attentional lapses and lower FD in the left SLF‐I. This finding indicates that the variation in the microstructure of a key frontoparietal white matter tract is associated with attentional lapses and may provide a trait‐like biomarker in the general population. However, SLF‐I microstructure alone does not explain propensity for attentional lapses, as other factors such as sleep deprivation or underlying psychological conditions (e.g., sleep disorders) may also lead to higher susceptibility in both healthy people and those with neurological disorders.
Publisher: Center for Open Science
Date: 20-11-2020
Abstract: Diffusion MRI has provided the neuroimaging community with a powerful tool to acquire in-vivo data sensitive to microstructural features of white matter, up to 3 orders of magnitude smaller than typical voxel sizes. The key to extracting such valuable information lies in complex modelling techniques, which form the link between the rich diffusion MRI data and various metrics related to the microstructural organisation. Over time, increasingly advanced techniques have been developed, up to the point where some diffusion MRI models can now provide access to properties specific to in idual fibre populations in each voxel in the presence of multiple "crossing" fibre pathways. While highly valuable, such fibre-specific information poses unique challenges for typical image processing pipelines and statistical analysis. In this work, we review the "fixel-based analysis" (FBA) framework that implements bespoke solutions to this end, and has recently seen a stark increase in adoption for studies of both typical (healthy) populations as well as a wide range of clinical populations. We describe the main concepts related to fixel-based analyses, as well as the methods and specific steps involved in a state-of-the-art FBA pipeline, with a focus on providing researchers with practical advice on how to interpret results. We also include an overview of the scope of current fixel-based analysis studies (until August 2020), categorised across a broad range of neuroscientific domains, listing key design choices and summarising their main results and conclusions. Finally, we critically discuss several aspects and challenges involved with the fixel-based analysis framework, and outline some directions and future opportunities.
Publisher: Elsevier BV
Date: 12-2019
DOI: 10.1016/J.CORTEX.2019.09.017
Abstract: The ability to understand the mental states of others - also known as Theory of Mind (ToM) - is critical for normal social interactions. We combine behavioural probes with structural and functional brain imaging to provide the first comprehensive analysis of ToM deficits following stroke using the Reading the Mind in the Eyes Test (RMET). First, fMRI was used to identify the functional brain network involved in a non-clinical cohort. Results indicated that, relative to a control task, the RMET increased activity in a widespread functional bilateral network comprising frontal and temporo-parietal areas. To investigate how damage to grey and white matter components of this network can lead to ToM impairment, parcel-based lesion-symptom mapping (PLSM), white-matter tract-wise statistical analysis (TSA) and disconnectome symptom mapping (DSM) were performed using structural images from 64 stroke patients. PLSM results revealed that low scores on the RMET were associated with damage centered around the right posterior frontal gyrus and insula. TSA and DSM results further revealed that low RMET scores were associated with damage to white-matter tracts connecting frontal and temporo-parietal components of the RMET functional network. Together, these findings suggest that making judgements about the mental states of others imposes demands on a large functional network that can easily be disrupted, both by damage to grey matter areas that form part of the network directly, or the white-matter pathways that connect them.
Publisher: Wiley
Date: 02-08-2014
DOI: 10.1002/HBM.22296
Publisher: Frontiers Media SA
Date: 29-01-2016
Publisher: Elsevier BV
Date: 05-2014
DOI: 10.1016/J.NBD.2014.01.013
Abstract: To investigate structural connectivity and the relationship between axonal microstructure and clinical, cognitive, and motor functions in premanifest (pre-HD) and symptomatic (symp-HD) Huntington's disease. Diffusion tensor imaging (DTI) data were acquired from 35 pre-HD, 36 symp-HD, and 35 controls. Structural connectivity was mapped between 40 brain regions of interest using tractography. Between-group differences in structural connectivity were identified using network based statistics. Radial diffusivity (RD) and fractional anisotropy (FA) were compared in the white matter tracts from aberrant networks. RD values in aberrant tracts were correlated with clinical severity, and cognitive and motor performance. A network connecting putamen with prefrontal and motor cortex demonstrated significantly reduced tractography streamlines in pre-HD. Symp-HD in iduals showed reduced streamlines in a network connecting prefrontal, motor, and parietal cortices with both caudate and putamen. The symp-HD group, compared to controls and pre-HD, showed both increased RD and decreased FA in the fronto-parietal and caudate-paracentral tracts and increased RD in the putamen-prefrontal and putamen-motor tracts. The pre-HDclose, compared to controls, showed increased RD in the putamen-prefrontal and fronto-parietal tracts. In the pre-HD group, significant negative correlations were observed between SDMT and Stroop performance and RD in the bilateral putamen-prefrontal tract. In the symp-HD group, RD in the fronto-parietal tract was significantly positively correlated with UHDRS motor scores and significantly negatively correlated with performance on SDMT and Stroop tasks. We have provided evidence of aberrant connectivity and microstructural integrity in white matter networks in HD. Microstructural changes in the cortico-striatal fibers were associated with cognitive and motor performance in pre-HD, suggesting that changes in axonal integrity provide an early marker for clinically relevant impairment in HD.
Publisher: Elsevier BV
Date: 2019
Publisher: Wiley
Date: 15-01-2015
DOI: 10.1002/BRB3.312
Publisher: Elsevier
Date: 2009
Publisher: BMJ
Date: 07-05-2016
Abstract: To measure iron accumulation in the basal ganglia in Huntington's disease (HD) using quantitative susceptibility mapping (QSM), and to ascertain its relevance in terms of clinical and disease severity. In this cross-sectional investigation, T2* weighted imaging was undertaken on 31 premanifest HD, 32 symptomatic HD and 30 control participants as part of the observational IMAGE-HD study. Group differences in iron accumulation were ascertained with QSM. Associations between susceptibility values and disease severity were also investigated. Compared with controls, both premanifest and symptomatic HD groups showed significantly greater iron content in pallidum, putamen and caudate. Additionally, iron accumulation in both putamen and caudate was significantly associated with disease severity. These findings provide the first evidence that QSM is sensitive to iron deposition in subcortical target areas across premanifest and symptomatic stages of HD. Such findings could open up new avenues for biomarker development and therapeutic intervention.
Publisher: Elsevier BV
Date: 07-2017
DOI: 10.1016/J.CORTEX.2017.04.001
Abstract: Neuropsychiatric disturbance-particularly executive dysfunction and behavioral dysregulation-is a common feature of Huntington's disease (HD), with implications for functional capacity and quality of life. No study to date has ascertained whether longitudinal change in brain activity is associated with neuropsychiatric deficits in HD. We used a set-response-shifting task together with functional magnetic resonance imaging to investigate 30-month longitudinal blood-oxygen level dependent (BOLD) signal changes in the fronto-striatal attentional control network in premanifest and symptomatic HD (pre-HD and symp-HD, respectively), relative to healthy control participants. We also assessed the extent to which changes in the BOLD signal over time were related to neuropsychiatric measures in the domains of executive dysfunction and behavioral dysregulation. Associations were also evaluated with clinical and disease severity. We found no longitudinal BOLD differences between pre-HD and controls over 30 months. In contrast, reduction in BOLD response over time was greater in symp-HD, relative to controls, in task-related areas (e.g., anterior cingulate cortex and striatum) and in regions from the default mode network (e.g., medial prefrontal cortex and posterior cingulate recuneus). Moreover, when considered across both premanifest and symptomatic stages, longitudinal BOLD signal decline in the right dorsolateral prefrontal cortex and putamen was associated with executive dysfunction and behavioral dysregulation measures. In addition, longitudinal reduction in BOLD signal, in fronto-striatal and default mode networks, correlated with disease severity. These results suggest that longitudinal change in fronto-striatal and default mode networks may be useful in understanding the biological underpinnings of functional decline in HD. Such findings offer new avenues for targeted treatments in terms of minimizing psychiatric impairment and potentially maximizing cognitive function.
Publisher: Springer Science and Business Media LLC
Date: 16-11-2015
DOI: 10.1007/S00429-013-0670-Z
Abstract: We characterized 30-month longitudinal change in functional activation and connectivity during working memory in premanifest (pre-HD) and symptomatic (symp-HD) Huntington's disease (HD). In a case-control longitudinal study (baseline, 18 months, and 30 months), we compared change in fMRI activity over time during working memory in 22 pre-HD, 11 symp-HD, and 20 control participants. Outcome measures were BOLD (blood-oxygen-level-dependent) activity during 1-BACK and 2-BACK working memory and functional connectivity between dorsolateral prefrontal cortex (DLPFC) and caudate. Compared with controls, the pre-HD group showed significantly increased activation longitudinally during 1-BACK in the left DLPFC and medial frontal cortex, and further increased activation during 2-BACK in the bilateral caudate, putamen, and temporal cortex. Longitudinal change in symp-HD was not significantly different from controls. Longitudinal changes in pre-HD were associated with disease burden and years to onset. The pre-HD group showed longitudinal decreased functional connectivity between left DLPFC and caudate during both 1-BACK and 2-BACK performance. We provide an evidence for longitudinal changes in BOLD activity during working memory prior to clinical manifestations of HD. The ability to increase activation in the prefrontal cortex over time may represent an early compensatory response during the premanifest stage, which may reflect an early marker for clinically relevant functional changes in HD.
Publisher: Wiley
Date: 27-02-2020
DOI: 10.1002/ACN3.50984
Publisher: Elsevier BV
Date: 02-2015
DOI: 10.1016/J.NBD.2014.12.009
Abstract: To quantify 18-month changes in white matter microstructure in premanifest (pre-HD) and symptomatic Huntington's disease (symp-HD). To investigate baseline clinical, cognitive and motor symptoms that are predictive of white matter microstructural change over 18months. Diffusion tensor imaging (DTI) data were analyzed for 28 pre-HD, 25 symp-HD, and 27 controls scanned at baseline and after 18months. Unbiased tract-based spatial statistics (TBSS) methods were used to identify longitudinal changes in fractional anisotropy (FA), radial diffusivity (RD), and axial diffusivity (AD) of white matter. Stepwise linear regression models were used to identify baseline clinical, cognitive, and motor measures that are predictive of longitudinal diffusion changes. Symp-HD compared to controls showed 18-month reductions in FA in the corpus callosum and cingulum white matter. Symp-HD compared to pre-HD showed increased RD in the corpus callosum and striatal projection pathways. FA in the body, genu, and splenium of the corpus callosum was significantly associated with a baseline clinical motor measure (Unified Huntington's Disease Rating Scale: total motor scores: UHDRS-TMS) across both HD groups. This measure was also the only independent predictor of longitudinal decline in FA in all parts of the corpus callosum across both HD groups. We provide direct evidence of longitudinal decline in white matter microstructure in symp-HD. Although pre-HD did not show longitudinal change, clinical symptoms and motor function predicted white matter microstructural changes for all gene positive subjects. These findings suggest that loss of axonal integrity is an early hallmark of neurodegenerative changes which are clinically relevant.
Publisher: Springer Science and Business Media LLC
Date: 11-03-2021
Publisher: Informa UK Limited
Date: 03-07-2017
Publisher: Cold Spring Harbor Laboratory
Date: 04-03-2022
DOI: 10.1101/2022.03.02.22271654
Abstract: Graph theoretical analysis of the structural connectome has been employed successfully to characterise brain network alterations in patients with traumatic brain injury (TBI). However, heterogeneity in neuropathology is a well-known issue in the TBI population, such that group comparisons of patients against controls are confounded by within-group variability. Recently, novel single-subject profiling approaches have been developed to capture inter-patient heterogeneity. We present a personalised connectomics approach that examines structural brain alterations in six chronic patients with moderate-to-severe TBI who underwent anatomical and diffusion magnetic resonance imaging (MRI). We generated in idualised profiles of lesion characteristics and network measures (including personalised graph metric ‘GraphMe’ plots, and nodal and edge-based brain network alterations) and compared them against healthy reference cases (N=12) to assess brain damage qualitatively and quantitatively at the in idual level. Our findings revealed clinically significant alterations of brain networks with high variability between patients. Our profiling can be used by clinicians to formulate a neuroscience-guided integrative rehabilitation program for TBI patients, and for designing personalised rehabilitation protocols based on their unique lesion load and connectome.
Publisher: Public Library of Science (PLoS)
Date: 30-03-2012
Publisher: Springer Netherlands
Date: 29-09-2014
Publisher: Elsevier BV
Date: 10-2013
DOI: 10.1016/J.BANDC.2013.07.004
Abstract: This study aimed to characterize, for the first time, 18 month longitudinal changes in both functional activation and functional connectivity during working memory in premanifest Huntington's disease (pre-HD) and symptomatic HD (symp-HD). Functional magnetic resonance imaging (fMRI) was used to investigate longitudinal changes in neuronal activity during working memory performance via an N-BACK task (0-BACK and 1-BACK) in 27 pre-HD, 17 symp-HD, and 23 control participants. Whole-brain analysis of activation and region-of-interest analysis of functional connectivity was applied to longitudinal fMRI data collected at baseline and 18 months follow-up. Compared with controls, the pre-HD group showed significantly increased activation longitudinally during 1-BACK versus 0-BACK in the lateral and medial prefrontal, anterior cingulate, primary motor, and temporal areas cortically, and caudate and putamen subcortically. Pre-HD far from onset, compared with controls, showed further longitudinal increases in the right and left dorsolateral prefrontal cortex (DLPFC). Longitudinal increased activation in anterior cingulate and medial primary motor areas were associated with disease burden in the pre-HD group. Moreover, in pre-HD increased activation over time in primary motor and putamen regions were associated with average response time during 1-BACK performance. During 1-BACK, functional connectivity between the right DLPFC and posterior parietal, anterior cingulate, and caudate was significantly reduced over 18months only in the pre-HD group. Longitudinal reductions in connectivity over 18 months may represent an early signature of cortico-cortical and cortico-striatal functional disconnectivity in pre-HD, whereas the concomitant increased cortical and subcortical activation may reflect a compensatory response to the demands for cognitive resources required during task performance. Our findings demonstrate that functional imaging modalities have the potential to serve as sensitive methods for the assessment of cortical and subcortical responses to future treatment measures.
Publisher: Elsevier BV
Date: 04-2017
DOI: 10.1016/J.MAD.2016.12.007
Abstract: Ageing is a poorly understood process of human development mired by a scientific approach that struggles to piece together distributed variable factors involved in ongoing transformations of living systems. Reconfiguring existing research paradigms, we review the concept of 'degeneracy', which has ergent popular and technical definitions. The technical meaning of degeneracy refers to the structural ersity underlying functional plasticity. Degeneracy is a distributed system property that can be observed within in idual brains or across different brains. For ex le, dementias with similar behavioural anomalies can result from a erse range of cellular "faults", which is an ex le of degeneracy because the symptoms are similar in spite of different underlying mechanisms. Degeneracy is a valuable epistemological tool that can transformatively enhance scientific models of bodily ageing. We propose that movement science is one of the first areas that can productively integrate degeneracy into models of bodily ageing. We also propose model organisms such as eusocial honey bees in which degeneracy can be studied at the molecular and cellular level. Developing a vocabulary for thinking about how distributed variable factors are interlinked is important if we are to understand bodily ageing not as a single entity, but as the heterogeneous construction of changing biological, social, and environmental processes.
No related grants have been discovered for Juan Fernando Dominguez Duque.