Our major interest is related to DNA damage response and oxidative stress during the presymptomatic and early-onset stages of Alzheimer’s disease. Oxidation-driven alterations target synapses and impair cognitive capacity.  In detail, we are interested in the role of BRCA1 protein in the pathogenesis of Alzheimer’s disease. We assumed that oxidative stress-induced activation of the BRCA1 protein in Alzheimer’s disease can both affect the processing of beta-amyloid by disrupting the function of presenilin 1 protein, as well it can induce neuronal death by cell cycle re-entry mechanism due to a faulty repair response to damaged DNA. To test this assumption, we will use neurons differentiated from induced pluripotent stem cells and fibroblasts from patients with various forms of Alzheimer’s disease. It will be both familial type, with partially recognized genetic background, associated with mutations in presenilin 1, and predominant sporadic type, which is much less understood.