These mice mimic fatal lysosomal storage disorders, such as Niemann pick types A and C, which lead to neurodegeneration, cognitive and psychiatric problems. The lipidic alterations we have found in these mice are similar to those reported in aging brains and may contribute to the cognitive decline that occurs as we age. In addition to the contribution to synaptic plasticity, research in the group has unveiled relevant roles of sphingomyelin and cholesterol in cellular processes such as autophagy, calcium homeostasis, or the establishment of axonal polarity in neurons as well as in microglia activation and oligodendrocyte differentiation. We preclinically assess pharmacological and genetic therapies to prevent/revert the consequences of lipid alterations. Recently, we are implementing in the lab the use of inducible pluripotent stem cells (iPSCs) from patients of lipidosis, and cerebral organoids to study lipid metabolism in the human context. The translational side of our research allows the generation of patents, the collaboration with pharma companies, the contact with patient associations and the participation in clinical trials. With our work we hope to contribute to understand and treat neurological diseases from childhood like Niemann Pick as well as neurodegenerative diseases related with aging such as Alzheimer.