Although the development of simpler models, as the ones shown in this work, constitutes a way to provide reliable answers in some pathological situations, these results must be validated on more physiological models such as primary cultures in order to check whether increasing either endogenously and/or exogenously the levels of Apo D could be a feasible intervention as part of medical therapy in neurodegenerative diseases. This evidence concerns the gene APOD and neurodegenerative disease.