Amyotrophic Lateral Sclerosis (LAS) is a rapidly fatal neurodegenerative disease that currently has no effective therapy. It is part of orphan diseases (incidence: 3-5 per 100,000 inhabitants). The Centre-Val de Loire region has about 300 patients and the increase in its incidence is a major public health problem. The recruitment of ALS patients to CHRU through the SLA Tours-Limoges Federation provides a cohort of approximately 350 ALS patients. Many treatments targeting different pathophysiological mechanisms have been studied in ALS, still unsuccessful for more than 50 years. Some molecules were promising in mice but had no beneficial therapeutic effect in humans. The methodology of preclinical and clinical trials is often called into question in a rush of haste and demands too ambitious in relation to the complexity and severity of this disease. In addition, the many physiopathological mechanisms involved and their interactions complex the therapeutic strategy. Intracellular protein aggregations are an integral part of the pathophysiology of the disease and represent a constant marker of ALS. Targeting these protein aggregations is thus a relevant therapeutic strategy. Beyond the specific mechanisms targeted in this project, the very concept of personalised treatment type intracorps has never been realised