Immunotherapy is one of the most promising treatment strategies for Alzheimer's disease despite the fact that large molecules, such as the antibodies used, are kept out of the brain by the blood-brain barrier. We have developed a core transporter protein that increases the uptake of antibodies in the mouse brain by almost 100 times and now want to continue our work on these projects in the following two steps: 1. transport into the human brain. Our brain transporter does not work in humans. There are viruses that infect the brain in both mice and humans. In order to do so, they must first cross the blood-brain barrier, so they have developed proteins on their surface that act as blood-brain barrier transporters. In this project, we will test whether these can be used to transport antibodies into the brain. 2. increase the brain's own degradation of amyloid beta. The treatment methods currently in clinical trials target the aggregates that have already been formed and do not bind to the smallest aggregates, which are perhaps the most toxic. If you can increase the brain's degradation of amyloid beta, you can prevent the aggregates from forming at all and then have a major effect on cognition. In this project, we try to activate the endogenous degradation by transporting the peptide somatostatin into the brain with our BBB transporter. There is enormous potential for improvement in immunotherapy and diagnostics of Alzheimer's disease and other brain diseases if we can significantly increase the uptake of antibodies in the brain and target new types of aggregates.