Attention Deficits
attention deficits
Axel Hutt
The new research team NECTARINE at INRIA in Strasbourg / France aims to create a synergy between clinicians and mathematical researchers to develop new healthcare technologies. The team works on stochastic microscopic network models to describe macroscopic experimental data, such as behavior and/or encephalographic. They collaborate closely with clinicians and choose their research focus along the clinical applications. Major scientific objectives are stochastic multi-scale simulations and mean-field descriptions of neural activity on the macroscopic scale. Moreover, merging experimental data and numerical models by machine learning techniques is an additional objective. The team's clinical research focuses on neuromodulation of patients suffering from deficits in attention and temporal prediction. The team offers the possibility to apply for a permanent position as Chargé de Recherche (CR) or Directeur de Recherche (DR) in the research field of mathematical neuroscience with a strong focus on stochastic dynamics linking brain network modelling with experimental data.
Organization of thalamic networks and mechanisms of dysfunction in schizophrenia and autism
Thalamic networks, at the core of thalamocortical and thalamosubcortical communications, underlie processes of perception, attention, memory, emotions, and the sleep-wake cycle, and are disrupted in mental disorders, including schizophrenia and autism. However, the underlying mechanisms of pathology are unknown. I will present novel evidence on key organizational principles, structural, and molecular features of thalamocortical networks, as well as critical thalamic pathway interactions that are likely affected in disorders. This data can facilitate modeling typical and abnormal brain function and can provide the foundation to understand heterogeneous disruption of these networks in sleep disorders, attention deficits, and cognitive and affective impairments in schizophrenia and autism, with important implications for the design of targeted therapeutic interventions
Mechanisms of CACNA1A-associated developmental epileptic encephalopathies
Developmental epileptic encephalopathies are early-onset epilepsies, often refractory to therapy, with developmental delay or regression. These disorders carry poor neurodevelopmental prognosis, with long-term refractory epilepsy and persistent cognitive, behavioral and motor deficits. Mutations in the CACNA1A gene, encoding the pore-forming α1 subunit of CaV2.1 voltage-gated calcium channels, result in a spectrum of neurological disorders, including severe, early-onset epileptic encephalopathies. Recent work from the Rossignol lab helped characterize the phenotypic spectrum of CACNA1A-related epilepsies in humans. Using conditional genetics and novel animal models, the Rossignol lab unveiled some of the underlying pathophysiological mechanisms, including critical deficits in cortical inhibition, resulting in seizures and a range of cognitive-behavioral deficits. Importantly, Dr. Rossignol’s team demonstrated that the targeted activation of specific GABAergic interneuron populations in selected cortical regions prevents motor seizures and reverts attention deficits and cognitive rigidity in mouse models of the disorder. These recent findings open novel avenues for the treatment of these severe CACNA1A-associated neurodevelopmental disorders.