The hallmark of Alzheimer’s disease is the appearance of insoluble and toxic protein deposits called amyloid plaques in the brain. Immune cells called microglia, which are found specifically in the brain, play a vital role in the removal of these pathological plaques. The TREM2 gene codes for the TREM2 protein, which is responsible for the activation of microglia and, as such, it is an important target for the development of novel approaches to the effective treatment of Alzheimer’s. To gain a more detailed understanding of the role of TREM2, a team of Munich neurobiologists led by SyNergy member Christian Haass (Professor of Metabolic Biochemistry at LMU Munich, Coordinator of the Munich Branch of the German Center for Neurodegenerative Diseases (DZNE) and a leading Alzheimer’s researcher) have now characterized the progression of the disease in mice in which the TREM2 gene had been deleted, and compared its course with that in normal mice.