Current biomedical research faces the challenge posed by the progressive aging of the population, which is inevitably accompanied by the development of metabolic and neurodegenerative diseases such as diabetes mellitus (DM) and Alzheimer's disease (AD). On the other hand, demyelination is a factor associated with brain aging that is closely linked to lipid metabolism. Metabolic disorders are risk factors for neurodegeneration and demyelination, and vice versa, as is the case for DM and AD. Both pathologies have in common chronic inflammation and dysregulation of the enzyme that degrades insulin (IDE). IDE is a multifunctional protease that participates in hepatic insulin clearance and regulates glucose homeostasis. Furthermore, IDE breaks down the A-beta peptide, a by-product of the proteolytic processing of the amyloid precursor protein, the accumulation of which in the brain causes inflammation and neuronal death, phenomena that are associated with AD. This processing of the A-beta peptide takes place in cell membranes, highly dependent on its subdomain structure (or lipid rafts) and its lipid composition. Apolipoproteins are found in these membrane subdomains that modulate their function and are potential protective agents.

Given the complexity and ignorance of the role of IDE, and of the molecular elements that accompany it in the membrane subdomains, in the etiology and pathogenesis of both types of diseases, we have brought together a multidisciplinary team of experts in cell biology and molecular, biochemistry and physiology of metabolism and the nervous system. Our teamwork is aimed at identifying new therapeutic targets that allow reestablishing metabolic control and cognitive abilities in neurodegenerative and demyelinating diseases.