Welcome to NEDI team

^{The NEDI team, from left to right : Andrea (PhD student), Fred (PI), Ana (postdoc) and Estelle (PhD student).}

Our Laboratory of Neural Differentiation (NEDI) did move beginning of January from Woluwe to the AMCB group at the LIBST institute ! Mainly using transgenic mice and chicken embryos as animal models, we investigate different aspects of the development, alterations and repair of the central nervous system, focusing on the spinal cord.

The CNS contains thousands of different types of neurons generated from a limited number of progenitor domains. Each neuronal type exhibits specific identity and defined localization that support its proper integration into adequate neural circuits. However, our understanding of the mechanisms that regulate neuronal differentiation and distribution during embryonic development, of their reactivation after nervous system injury, and of the contribution of specific neuronal populations to certain neurodegenerative pathologies remains largely incomplete.

Three research lines are followed in the lab. First, we try to identify molecular and cellular mechanisms that regulate the earlier steps of neuronal development in the spinal cord, namely the subdivision of large initial populations into multiple specialized subsets (a process we call neuronal diversification) and the migration of each subset to its final location. We previously identified numerous transcription factors regulating these processes, and we are now deciphering their downstream effectors. We also characterize neuronal populations of the spinal cord that are yet unknown and try to determine their contribution to the formation and activity of the spinal locomotor circuits. Finally, we uncovered a non-cell autonomous mechanism that coordinate the development of different neuronal subsets, and identified now the molecular signals involved.

However, it is known for ~20 years now that any lesion of the CNS results in the reactivation of developmental processes, including proliferation, differentiation, migration, axonal growth and formation of new synapses, that are normally silent or restricted in the adult. In a second set of projects, we investigate the reactivation of developmental mechanisms after adult spinal cord injury, the neo-production of specific neural populations and their possible contribution to tissue repair and functional recovery.

Finally, we will soon initiate a new research project to evaluate the contribution of spinal interneurons to the initiation or the progression of Amyotrophic Lateral Sclerosis (ALS), a devastating neurodegenerative disorder characterized by the progressive loss of spinal motor neuron and progressive paralysis. ALS is classically described as a motor neuron disease, although the contribution of glial cells (astrocytes and oligodendrocytes) has already been demonstrated. More recently, evidence emerged that spinal interneurons could be affected before, and could even be responsible for, the degeneration of motor neurons. Using the genetic tools that we developed to investigate spinal interneuron development, we will assess the contribution of these neuronal populations to the onset and progression of the disease.

Please feel welcome to visit us at the A0 level of the Carnoy building for a scientific discussion, technical exchanges or to have a drink together !