Alzheimer's disease is one of the most common dementias and a growing challenge for both healthcare and society. In recent years, research has shown that the brain's immune cells, microglia, play a crucial role in the development of the disease. Rather than just protecting the brain, microglia can in some situations drive harmful inflammation that worsens the disease. In our previous research, we were the first to show that the protein galectin-3 (gal3) has a direct harmful effect in Alzheimer's. We were able to demonstrate this both through genetic analyses, studies of brain tissue and spinal fluid from patients, and in experimental disease models. Together with colleagues in Lund, we are now developing drugs that block galectin-3, and some of these are already being tested clinically. The aim of our project is to deepen the understanding of how galectin-3 directs microglia towards harmful behavior. We will use advanced techniques such as single-cell analysis of genes and proteins to map changes in microglia. We will use this knowledge to test new gal3 inhibitors, first in cell cultures and then in animal models. We expect to identify common mechanisms that drive microglia in Alzheimer's. This will not only allow us to better understand the disease but also provide a basis for new drugs. Our research is directly relevant to future clinical trials of galectin-3 inhibitors and may eventually contribute to more effective treatments for patients with Alzheimer's.