Neurodegenerative diseases such as Alzheimer's and Parkinson's affect millions of people in the world and requires extensive care and cause premature death. Despite great efforts, we do not understand the diseases and we have no cure. The disorders are characterized by the formation of hallmark protein inclusions. Evidence suggests that intracellular, oligomeric forms of these proteins precede aggregate formation, promote pathology, and spread the disease in a prion-like manner.
Me and my research team want to understand why the nervous cells in the brain get sick and how the disease is spread in the brain. To do that, we investigate the cellular mechanisms of propagation and we have developed advanced models and tools to study the neuron-to-neuron spread. With these we address questions like: What happens to the connections between the nerve cells? How does the recipient cell become ill? Can these events be used as diagnostic tools? Could we slow down the disease propagation?
Through this research, we have made important breakthroughs where we could show that toxic protein aggregates can spread between neurons in Alzheimer's and Parkinson's disease. Recently, my research team has shown the cellular mechanism that spread Alzheimer’s disease to new brain areas. In cultured cells we could even inhibit this disease propagation. We have also shown that the capacity of the cell's degradation system is decisive for the effect of this spread on the receiving cell.
Understanding the mechanisms causing spreading and damage to new cells is necessary. By combining questions from the clinic with advanced research methods, the projects my research group are working with has the potential to find these mechanisms and through new understanding of the mechanisms of the disease, the projects can provide new possibilities for diagnostics and drug development.
