Axel Nimmerjahn
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Axel Nimmerjahn completed his Boehringer Ingelheim Fonds-supported Ph.D. in physics in the laboratories of Fritjof Helmchen and Bert Sakmann at the Max Planck Institute for Medical Research/University of Heidelberg, Germany. Following his Alexander von Humboldt and Human Frontier Science Program-supported postdoctoral training with Mark Schnitzer and Ben Barres at Stanford University, he joined the Salk Institute for Biological Studies in the Waitt Advanced Biophotonics Center. Nimmerjahn’s work has been recognized by a variety of awards, including the Du Bois-Reymond Award of the German Physiologic Society, the Otto Hahn Medal and Award of the Max Planck Society, and the DP2/New Innovator and EUREKA Awards of the National Institutes of Health.
The human central nervous system (CNS) consists of an incredibly diverse set of cells, and each cell type carries out highly specialized functions in cellular networks of dazzling complexity. While much research has focused on understanding the circuits formed by neurons, brain cells called glia are equally pervasive and account for roughly an equal number of cells in the human CNS. Glial cells were long believed to play a merely passive, supportive role. However, it is becoming increasingly clear that glia make crucial contributions to CNS formation, operation and adaptation. Additionally, glial cells are involved in practically all CNS injuries and diseases. This makes glia promising targets for future therapeutic interventions. Nimmerjahn’s lab has spearheaded the development of new microscopy techniques to visualize the dynamics of glial cells and their functional cellular interactions in the living CNS. His team has worked to shrink the size of microscopes to make them wearable, allowing them to reveal how cellular activity relates to animal behavior. They have created new tools for cell type-specific staining and genetic manipulation and for analysis of large-scale imaging data. This has allowed them to address long-standing questions regarding the role of glia in the intact healthy and diseased CNS.