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

Alzheimer’s disease is the sixth leading cause of death, but unfortunately one of those without an effective treatment. While number of deaths from cancers, heart disease, strokes and HIV continues to decline, those from Alzheimer’s disease have increased by 68% over the last 10 years. That is why in this project we search for new players in the pathogenesis of Alzheimer’s disease, that could be potential targets for the effective causative treatment. One such candidate, based on our and other researchers’ preliminary results, is the BRCA1 protein. This exciting research target is a very likely causative factor in Alzheimer’s disease. We believe that it may become an effective therapeutic goal. We choose BRCA1 not only on the basis of our previous transcriptomic results but also due to recently more pronounced belief that tumorigenesis and neurodegeneration represent two sides of the same coin.

We want to find out what might be 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.