Cellular protein scientist Stefan Rüdiger has been granted funding by Alzheimer Nederland. He will receive € 200,000 for research on the aggregation of the Tau protein, a hallmark of Alzheimer’s disease. He aims to develop a chaperone-mimetic removal strategy for Tau aggregation.
The hallmark of Alzheimer's disease is the death of neurons caused by aggregation of the Tau protein in the brain. Key is the formation of fibrils: long needle-like protein aggregates. “Tau proteins are continuously present in the brain, but are normally disassembled by chaperones. It is unclear, however, why these Tau fibrils are no longer disassembled at a certain age”, says Stefan Rüdiger of the section Cellular Protein Chemistry at Utrecht University. “We will provide a new strategy to deal with Alzheimer aggregates inside neurons, by exploiting nature’s own defense system. We hypothesize that chaperone-like compounds allow regaining control on Tau aggregation.”
To date there is no causal cure of Alzheimer's disease, largely because of lack of knowledge at molecular level. Rüdiger aims to provide a key step in molecular understanding of aggregation control of Tau, and pave the way for a new strategy for target Alzheimer. “I feel very honoured to receive this grant from Alzheimer Nederland. This is really where people on the streets donate their money for. Understanding the disease is essential to work a cure.”