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  • Simultaneous EEG-fNIRS reveals how age and feedback affects motor imagery signatures

    15 June 2018

    Stroke frequently results in motor impairment. Motor imagery (MI), the mental practice of movements, has been suggested as a promising complement to other therapeutic approaches facilitating motor rehabilitation. Of particular potential is the combination of MI with neurofeedback (NF). However, MI NF protocols have been largely optimized only in younger healthy adults, although strokes occur more frequently in older adults. The present study examined the influence of age on the neural correlates of MI supported by electroencephalogram (EEG)-based NF and on the neural correlates of motor execution. We adopted a multimodal neuroimaging framework focusing on EEG-derived event-related desynchronization (ERD%) and oxygenated (HbO) and deoxygenated hemoglobin (HbR) concentrations simultaneously acquired using functional near-infrared spectroscopy (fNIRS). ERD%, HbO concentration and HbR concentration were compared between younger (mean age: 24.4 years) and older healthy adults (mean age: 62.6 years). During MI, ERD% and HbR concentration were less lateralized in older adults than in younger adults. The lateralization-by-age interaction was not significant for movement execution. Moreover, EEG-based NF was related to an increase in task-specific activity when compared to the absence of feedback in both older and younger adults. Finally, significant modulation correlations were found between ERD% and hemodynamic measures despite the absence of significant amplitude correlations. Overall, the findings suggest a complex relationship between age and movement-related activity in electrophysiological and hemodynamic measures. Our results emphasize that the age of the actual end-user should be taken into account when designing neurorehabilitation protocols.

  • Lateralization patterns of covert but not overt movements change with age: An EEG neurofeedback study.

    14 June 2018

    The mental practice of movements has been suggested as a promising add-on therapy to facilitate motor recovery after stroke. In the case of mentally practised movements, electroencephalogram (EEG) can be utilized to provide feedback about an otherwise covert act. The main target group for such an intervention are elderly patients, though research so far is largely focused on young populations (<30 years). The present study therefore aimed to examine the influence of age on the neural correlates of covert movements (CMs) in a real-time EEG neurofeedback framework. CM-induced event-related desynchronization (ERD) was studied in young (mean age: 23.6 years) and elderly (mean age: 62.7 years) healthy adults. Participants performed covert and overt hand movements. CMs were based on kinesthetic motor imagery (MI) or quasi-movements (QM). Based on previous studies investigating QM in the mu frequency range (8-13Hz) QM were expected to result in more lateralized ERD% patterns and accordingly higher classification accuracies. Independent of CM strategy the elderly were characterized by a significantly reduced lateralization of ERD%, due to stronger ipsilateral ERD%, and in consequence, reduced classification accuracies. QM were generally perceived as more vivid, but no differences were evident between MI and QM in ERD% or classification accuracies. EEG feedback enhanced task-related activity independently of strategy and age. ERD% measures of overt and covert movements were strongly related in young adults, whereas in the elderly ERD% lateralization is dissociated. In summary, we did not find evidence in support of more pronounced ERD% lateralization patterns in QM. Our finding of a less lateralized activation pattern in the elderly is in accordance to previous research and with the idea that compensatory processes help to overcome neurodegenerative changes related to normal ageing. Importantly, it indicates that EEG neurofeedback studies should place more emphasis on the age of the potential end-users.

  • Real-time EEG feedback during simultaneous EEG-fMRI identifies the cortical signature of motor imagery.

    31 May 2018

    Motor imagery (MI) combined with real-time electroencephalogram (EEG) feedback is a popular approach for steering brain-computer interfaces (BCI). MI BCI has been considered promising as add-on therapy to support motor recovery after stroke. Yet whether EEG neurofeedback indeed targets specific sensorimotor activation patterns cannot be unambiguously inferred from EEG alone. We combined MI EEG neurofeedback with concurrent and continuous functional magnetic resonance imaging (fMRI) to characterize the relationship between MI EEG neurofeedback and activation in cortical sensorimotor areas. EEG signals were corrected online from interfering MRI gradient and ballistocardiogram artifacts, enabling the delivery of real-time EEG feedback. Significantly enhanced task-specific brain activity during feedback compared to no feedback blocks was present in EEG and fMRI. Moreover, the contralateral MI related decrease in EEG sensorimotor rhythm amplitude correlated inversely with fMRI activation in the contralateral sensorimotor areas, whereas a lateralized fMRI pattern did not necessarily go along with a lateralized EEG pattern. Together, the findings indicate a complex relationship between MI EEG signals and sensorimotor cortical activity, whereby both are similarly modulated by EEG neurofeedback. This finding supports the potential of MI EEG neurofeedback for motor rehabilitation and helps to better understand individual differences in MI BCI performance.

  • Genetic screening in sporadic ALS and FTD.

    15 June 2018

    The increasing complexity of the genetic landscape in amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) presents a significant resource and physician training challenge. At least 10% of those diagnosed with ALS or FTD are known to carry an autosomal dominant genetic mutation. There is no consensus on what constitutes a positive family history, and ascertainment is unreliable for many reasons. However, symptomatic individuals often wish to understand as much as possible about the cause of their disease, and to share this knowledge with their family. While the right of an individual not to know is a key aspect of patient autonomy, and despite the absence of definitive therapy, many newly diagnosed individuals are likely to elect for genetic testing if offered. It is incumbent on the practitioner to ensure that they are adequately informed, counselled and supported in this decision.

  • Mutations in the vesicular trafficking protein annexin A11 are associated with amyotrophic lateral sclerosis.

    15 June 2018

    Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder. We screened 751 familial ALS patient whole-exome sequences and identified six mutations including p.D40G in the ANXA11 gene in 13 individuals. The p.D40G mutation was absent from 70,000 control whole-exome sequences. This mutation segregated with disease in two kindreds and was present in another two unrelated cases (P = 0.0102), and all mutation carriers shared a common founder haplotype. Annexin A11-positive protein aggregates were abundant in spinal cord motor neurons and hippocampal neuronal axons in an ALS patient carrying the p.D40G mutation. Transfected human embryonic kidney cells expressing ANXA11 with the p.D40G mutation and other N-terminal mutations showed altered binding to calcyclin, and the p.R235Q mutant protein formed insoluble aggregates. We conclude that mutations in ANXA11 are associated with ALS and implicate defective intracellular protein trafficking in disease pathogenesis.

  • Influence of the blood-CSF-barrier function on S100B in neurodegenerative diseases.

    26 April 2018

    OBJECTIVES: S100B was proposed to be a CSF and blood biomarker in a number of neurological diseases. The route of S100B to the CSF and the blood in neurodegenerative diseases is unclear. To assess the impact of the physiological or impaired blood-CSF-barrier (BCSFB) function on S100B concentrations in CSF and serum, we analysed S100B in correlation of the albumin quotient. MATERIALS AND METHODS: S100Bserum and S100BCSF were quantified in samples from patients with a variety of neurological diseases using an immunoluminometric assay (Sangtec LIA-mat). Measures were analysed for a potential relation to the CSF/serum-albumin quotient (Qalb ), which indicates the BCSFB functionality. RESULTS: We reasserted increased S100B concentrations in CSF and serum of CJD patients. Elevated S100Bserum correlated with elevated S100BCSF in all diagnoses but with exceptions. Neither S100BCSF nor S100Bserum did correlate with Qalb , even when the BCSFB function was progressively impaired as demonstrated by increased Qalb . CONCLUSIONS: The lack of correlation between Qalb and S100BCSF is typically seen for proteins which are brain derived. Therefore, we propose that S100B enters the blood with the bulk flow via Pacchioni's granules and along the spinal nerve sheaths.

  • Limited role of free TDP-43 as a diagnostic tool in neurodegenerative diseases.

    14 June 2018

    TAR DNA-binding protein 43 (TDP-43) is one of the neuropathological hallmarks in amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD). It is present in patients' blood and cerebrospinal fluid (CSF); however, the source and clinical relevance of TDP-43 measurements in body fluids is uncertain. We investigated paired CSF and serum samples, blood lymphocytes, brain urea fractions and purified exosomes from CSF for TDP-43 by one- (1D), and two-dimensional (2D) Western immunoblotting (WB) and quantitative mass spectrometry (MRM) in patients with ALS, FTLD and non-neurodegenerative diseases. By means of 2D-WB we were able to demonstrate a similar isoform pattern of TDP-43 in lymphocytes, serum and CSF in contrast to that of brain urea fractions with TDP-43 pathology. We found that the TDP-43 CSF to blood concentration ratio is about 1:200. As a possible brain specific fraction we found TDP-43 in exosome preparations from CSF by immunoblot and MRM. We conclude that TDP-43 in CSF originates mainly from blood. Measurements of TDP-43 in CSF and blood are of minor importance as a diagnostic tool, but may be important for monitoring therapy effects of TDP-43 modifying drugs.

  • Cognitive Neurology Research Group

    4 March 2013

    DCN

    We want to understand how - and why - brain function can be disturbed to lead to inattention, poor memory and abnormal decision making. Our aim is to develop new treatments for these conditions across a range of neurological disorders.

  • Neuroanatomy and Cognition Group

    15 January 2013

    DCN

    Our projects study cognitive/psychiatric disorders and comparative evolutionary neuroscience. We are interested in the relationship between brain structure and function in disease, development and aging - particularly related to language and social cognition.

  • Epilepsy Imaging Research Group

    14 February 2013

    FMRIB

    Combining state-of-the-art brain imaging methods, we aim to understand how functional networks in the brain respond and adapt to epilepsy and epilepsy-associated lesions.

  • Clinical Ophthalmology Research Group

    15 January 2013

    NLO

    We are developing gene therapy and stem cell treatments for retinal diseases

  • Retinal Neurobiology and Optogenetics Group

    15 January 2013

    NLO

    Our research focuses on light dependent signalling in the retina and brain, including visual and non-visual light detection. We are also examining novel opsin photopigments and exploring their applications to optogenetics.

  • Retinal Degeneration and Gene Identification

    15 January 2013

    NLO

    Our work involves the identification and characterisation of genes that play a role in the retina, including both visual and non-image forming tasks such as the detection of light for the entrainment of the circadian system.

  • Molecular Neurodegeneration Research Group

    11 March 2014

    DCN

    Our aim is to understand fundamental biological processes that could inform the development of targeted therapies and innovative biomarkers in neurodegenerative and neurogenetic disorders.

  • FMRIB Plasticity Group

    15 January 2013

    FMRIB

    We study how the brain changes when we learn, as we get older, or when we recover damage such as stroke. We use brain imaging to monitor brain change and we aim to develop new approaches to facilitate learning, recovery and healthy ageing.