Researchers from the Cell Signaling and Apoptosis group at Vall d’Hebron Institute of Research (VHIR), led by Dr. Joan Comella, have discovered that a neuronal protein, the long isoform of FAIM-L (Fas Apoptotic Inhibitory Molecule) protects from apoptosis or programmed cell death, by regulating one of the Inhibitor of Apoptosis Proteins, called XIAP. The groundbreaking research has been published in The Journal of Neuroscience.Apoptosis is a physiological process that regulates the number of cells in the body, by eliminating those that are overexpressed, injured, or have transient functions. It plays an important role in neurodegenerative diseases, because its overexpression causes cell death, as well as in cancer, because its inhibition triggers the tumor progression. XIAPs are the most potent caspase inhibitor in vitro and their levels are decreased in neurodegenerative diseases such as Alzheimer’s disease. In this study, VHIR researchers discovered the link of these inhibitors with the neuronal protein FAIM-L, which was previously reported as a protector from neuronal death. Specifically, they have identified in mice that FAIM-L protects the degradation of XIAP, impeding the apoptosis activation and then, allowing the neuronal survival. With this results, Dr. Comella expects that “the use of FAIM-L as an XIAP ‘guardian’ might not be restricted to the nervous system and deserves to be exploted in other systems with deleterious cell death, such as auto-immune diseases”.Dr. Rana S. Moubaraq, who is currently working at the "http://skirball.med.nyu.edu/" Skirball Institute of Biomolecular Medicine in New York, is the first author of this study that opens the door to further research in new drugs against neurodegenerative diseases.