Increasing evidence suggests that dysregulation of lipid metabolism is associated with neurodegeneration in brain disorders such as Alzheimer's and Parkinson's diseases.
Lipid storage organelle (lipid droplets, LDs), accumulate in many cell types in response to stress and it is now clear that LDs function not only as lipid stores but also as dynamic regulators of the stress response. We recently showed that dFatp (Drosophila fatty acid transport protein) is required and sufficient LD formation in retinal pigment cells (RPCs) and that FATP-mediated LD formation in RCPs promotes neuronal homeostasis (Van Den Brink et al. 2018). Furthermore, we used a Drosophila expressing alpha-synuclein as model of Parkinson's disease (PD) in which we observed a neuronal accumulation of LD in Drosophila. During the seminar, I will discuss the mechanism leading to LD accumulation and its pathological relevance in neurodegeneration.