Our mission is to unveil molecular mechanisms triggering neurons death in Alzheimer’s disease and other neurodegenrative disorders.

We work on the molecular pathomechanisms of neuronal death underlying the role of oxidative stress and DNA damage response (DDR) with the major role of BRCA1. We use induced pluripotent stem (iPS) cells reprogrammed from fibroblasts derived from Alzheimer’s disease (AD) patients. iPS cells are induced into neuroepithelial-like stem cells (NES) and differentiated  to neurons. In our collection we have more than 30 cell lines derived from familial early-onset Alzheimer’s disease (fEOAD) patients carrying mutations in PSEN1, encoding presenilin 1, the enzymatic core of gamma secretase complex processing beta-amyloid, major pathological hallmark of AD. Our DDR-based studies conducted using patients-derived neuronal model aim to provide a molecular link between beta-amyloid pathology and multifactorial stress occuring at presymptomatic phase or at the very early onset of AD.