Our mission is to 1) understand how the cellular environment contributes to the degeneration of motoneurons in amyotrophic lateral sclerosis (ALS) and other motoneuron disorders
2) develop new therapeutic strategies.
Our research is carried out by a multidisciplinary team of neurobiologists, electrophysiologists, immunologists, clinicians, and geneticists.
Reactive astrocytes, microglia and invading lymphocytes in the vicinity of motoneurons play a pivotal role during the pathogenic process by defining a neuroinflammatory context. We propose an interdisciplinary approach to investigate the extrinsic determinants of motoneuron degeneration.
Abnormal excitability of motoneurons and synaptic transmission is a common pathogenic feature of ALS and SMA. Our research efforts are directed to investigate the molecular determinants of aberrant electrical activity of motoneurons in the disease
Our goal is to integrate the knowledge gained by basic research in a translational perspective. Our research focuses on the completion of our preclinical investigations by studies of human biological specimens, genetic association and functional studies. Reciprocally, clinical and genetic research open new pre-clinical research field.
ADELE aims at exploring the spatiotemporal dynamics of spinal network activity during post-natal development of an ALS mouse model. We propose to combine complementary areas of expertise to answer a question that has never been functionally addressed before: is ALS a developmental disease that originates when spinal circuits are first established and remains silent before reaching a clinical breakthrough point? This conceptual paradigm shift requires a scientifically robust proof of concept in order to stimulate new examination protocols aimed to reveal early preclinical markers of the disease raising an alert towards early ALS diagnostics, to guide screening of genetic background in the cohort of patients with a risk of ALS development, and will open large time window for the new treatments preventing the disease.