My long-term research focus is on the effect of neuroinflammation on triggering and progression of neurodegeneration. Specifically I am interested in how brain damage affects glial function in cell autonomous way and neuron-glia communication through non-cell autonomous pathways. Answers to these outstanding questions can be implemented together with information on the contribution of genetics to disease in particular patients, which will let us propose novel personalized ways to tackle pathological changes in Alzheimer’s disease (AD). I am a molecular and cellular biologist with 9+ years of experience in validation of potential targets for treatment of AD using cell lines, primary culture and mouse models – uniquely qualified to fulfill these goals. As a predoctoral student with Prof. Bart De Strooper (KU Leuven, Belgium) I used agonists of serotonergic receptors to modulate production of amyloid-beta peptide and test the amyloid cascade hypothesis.
I discovered the signaling pathway leading to the activation of alpha-secretase and how this effect is beneficial against pathological and behavioral changes in AD mouse model. For my postdoctoral training I chose to work on genetic risk factors for AD with Prof. Alison Goate (ISSMS, New York, US). I have implemented different assays in the lab, e.g. phagocytosis, apoptosis, etc. for validation of AD risk factors in cell lines, co-cultures of microglia with primary or iPSc-derived neurons and astrocytes, and mouse models of brain damage. I thrive in a collaborative environment created at the Loeb Center for Alzheimer’s disease and have successfully accomplished several projects as evidenced by recent publications