Every 3 seconds, someone in the world develops dementia. Presently, more than 55 million people worldwide are living with dementia and this number is predicted to double every two decades due to ageing populations. Critically, there is currently no cure nor effective treatment options to prevent or reverse the loss of brain cells that drives diseases associated with dementia and neurodegeneration.

We believe that, dissecting the molecular principles of selective cellular vulnerability underlying these diseases is key to unlock new therapeutic approaches for patients and, is now possible due to remarkable technological advancements in recent years. We have been developing and implementing new in-vitro human models of disease (iPSC-patient derived), gene-editing tools at scale (genetic CRISPR screens) and -omics approaches with single cell and spatial resolution (transcriptomics and lipidomics) to understand the selective nature of neuronal dysfunction.

Neurons are amongst the most highly specialised cells in the human body and require remarkable metabolic adaptations. In this talk I will give insights on our work elucidating the role of lipid metabolism in neuronal dysfunction, on the identification of novel factors regulating neuronal vulnerability and resilience, and the quest to dissect functional neuronal heterogeneity.