50 research outputs found

    A user-centred approach to unlock the potential of non-invasive BCIs: an unprecedented international translational effort

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    Non-invasive Mental Task-based Brain-Computer Interfaces (MT-BCIs) enable their users to interact with the environment through their brain activity alone (measured using electroencephalography for example), by performing mental tasks such as mental calculation or motor imagery. Current developments in technology hint at a wide range of possible applications, both in the clinical and non-clinical domains. MT-BCIs can be used to control (neuro)prostheses or interact with video games, among many other applications. They can also be used to restore cognitive and motor abilities for stroke rehabilitation, or even improve athletic performance.Nonetheless, the expected transfer of MT-BCIs from the lab to the marketplace will be greatly impeded if all resources are allocated to technological aspects alone. We cannot neglect the Human End-User that sits in the centre of the loop. Indeed, self-regulating one’s brain activity through mental tasks to interact is an acquired skill that requires appropriate training. Yet several studies have shown that current training procedures do not enable MT-BCI users to reach adequate levels of performance. Therefore, one significant challenge for the community is that of improving end-user training.To do so, another fundamental challenge must be taken into account: we need to understand the processes that underlie MT-BCI performance and user learning. It is currently estimated that 10 to 30% of people cannot control an MT-BCI. These people are often referred to as “BCI inefficient”. But the concept of “BCI inefficiency” is debated. Does it really exist? Or, are low performances due to insufficient training, training procedures that are unsuited to these users or is the BCI data processing not sensitive enough? The currently available literature does not allow for a definitive answer to these questions as most published studies either include a limited number of participants (i.e., 10 to 20 participants) and/or training sessions (i.e., 1 or 2). We still have very little insight into what the MT-BCI learning curve looks like, and into which factors (including both user-related and machine-related factors) influence this learning curve. Finding answers will require a large number of experiments, involving a large number of participants taking part in multiple training sessions. It is not feasible for one research lab or even a small consortium to undertake such experiments alone. Therefore, an unprecedented coordinated effort from the research community is necessary.We are convinced that combining forces will allow us to characterise in detail MT-BCI user learning, and thereby provide a mandatory step toward transferring BCIs “out of the lab”. This is why we gathered an international, interdisciplinary consortium of BCI researchers from more than 20 different labs across Europe and Japan, including pioneers in the field. This collaboration will enable us to collect considerable amounts of data (at least 100 participants for 20 training sessions each) and establish a large open database. Based on this precious resource, we could then lead sound analyses to answer the previously mentioned questions. Using this data, our consortium could offer solutions on how to improve MT-BCI training procedures using innovative approaches (e.g., personalisation using intelligent tutoring systems) and technologies (e.g., virtual reality). The CHIST-ERA programme represents a unique opportunity to conduct this ambitious project, which will foster innovation in our field and strengthen our community

    Redundant Mechanisms for Regulation of Midline Crossing in Drosophila

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    During development, all neurons have to decide on whether to cross the longitudinal midline to project on the contralateral side of the body. In vertebrates and invertebrates regulation of crossing is achieved by interfering with Robo signalling either through sorting and degradation of the receptor, in flies, or through silencing of its repulsive activity, in vertebrates. Here I show that in Drosophila a second mechanism of regulation exists that is independent from sorting. Using in vitro and in vivo assays I mapped the region of Robo that is sufficient and required for its interaction with Comm, its sorting receptor. By modifying that region, I generated new forms of Robo that are insensitive to Comm sorting in vitro and in vivo, yet still able to normally translate repulsive activity in vivo. Using gene targeting by homologous recombination I created new conditional alleles of robo that are sorting defective (roboSD). Surprisingly, expression of these modified proteins results in phenotypically normal flies, unveiling a sorting independent mechanism of regulation

    Effects of IKAP/hELP1 Deficiency on Gene Expression in Differentiating Neuroblastoma Cells: Implications for Familial Dysautonomia

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    Familial dysautonomia (FD) is a developmental neuropathy of the sensory and autonomous nervous systems. The IKBKAP gene, encoding the IKAP/hELP1 subunit of the RNA polymerase II Elongator complex is mutated in FD patients, leading to a tissue-specific mis-splicing of the gene and to the absence of the protein in neuronal tissues. To elucidate the function of IKAP/hELP1 in the development of neuronal cells, we have downregulated IKBKAP expression in SHSY5Y cells, a neuroblastoma cell line of a neural crest origin. We have previously shown that these cells exhibit abnormal cell adhesion when allowed to differentiate under defined culture conditions on laminin substratum. Here, we report results of a microarray expression analysis of IKAP/hELP1 downregulated cells that were grown on laminin under differentiation or non-differentiation growth conditions. It is shown that under non-differentiation growth conditions, IKAP/hELP1 downregulation affects genes important for early developmental stages of the nervous system, including cell signaling, cell adhesion and neural crest migration. IKAP/hELP1 downregulation during differentiation affects the expression of genes that play a role in late neuronal development, in axonal projection and synapse formation and function. We also show that IKAP/hELP1 deficiency affects the expression of genes involved in calcium metabolism before and after differentiation of the neuroblastoma cells. Hence, our data support IKAP/hELP1 importance in the development and function of neuronal cells and contribute to the understanding of the FD phenotype

    Modulators of axonal growth and guidance at the brain midline with special reference to glial heparan sulfate proteoglycans

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