Alicia is currently the cell biologist for the spin-out company, MeOmics. MeOmics is focused on transforming mental health, culturing iPSC from schizophrenia patients and differentiating the cells into glutamatergic neurons via a defined protocol to seed onto the Axion MEA system. MeOmics aims to see differences between patients and controls, and to test a range of known and in-development drugs on the cells themselves with the goal to help transfer treatments and our understanding of mental health.

Elliot obtained his PhD in Chemical Biology and Drug Discovery from Leiden University in the Netherlands. His research involved the development of novel chemical tools and inhibitors to study the endocannabinoid system in the brain and periphery. He discovered the first brain-active inhibitor for the enzyme NAPE-PLD, which produces the endocannabinoid anandamide, that can modulate stress and fear memory. His PhD work inspired Elliot to change disciplines and study the molecular mechanisms of neurological disease. He moved to the lab of Professor Richard Wade-Martins at the University of Oxford as a Dutch Research Council (NWO) Rubicon fellow to study the connection between alpha-synuclein, mitochondrial and neuronal dysfunction in Parkinson’s disease (PD) using induced pluripotent stem cell (iPSC)-derived dopaminergic neurons from PD patients and applying these on multi-electrode arrays. Elliot is currently working as an Oxford-Janssen Fellow where he will investigate resilience in Alzheimer’s disease using iPSC-derived cortical neurons from patients from the Deep and Frequent Phenotyping (DFP) study.

In recent years, Eugeni has been working with Pietro Fratta to characterize the aberrant splicing that occurs in the disease process of ALS/FTD. A large portion of their research is focused on investigating cryptic splicing in the UNC13A gene following loss of TDP-43, a hallmark of ALS-FTD. They are also interested in the functional effects of UNC13A loss in the context of TDP-43 knockdown, and is currently investigating how neuronal synchrony is affected when these two proteins are lost as well as the extent of their importance to ALS-FTD pathogenesis.