Dr. Strittmatter has a long-standing interest in ligand–receptor and signal transduction interactions in translational neuroscience. He developed expertise in the biochemistry of neuronal receptors during MD/PhD training with Solomon Snyder at Johns Hopkins. He pursued Neurology residency training at Massachusetts General Hospital under the guidance of John B. Martin, Raymond Adams, and C. Miller Fischer. His clinical practice included an early focus on Movement Disorders working with John Growdin and Kenneth Marek. Recently, he founded the Yale Memory Disorders Clinic leading 4 neurologists plus support personnel. After Residency training, he developed an interest in the molecular biology of axon growth during a Fellowship with Mark Fishman. In his own laboratory at Yale, the mechanisms of axon guidance were the first focus, and insights into the molecular mechanisms of Semaphorin action during brain development were revealed. This led to an interest in the molecular pathways that inhibit fiber growth and functional rewiring of healthy and damaged adult brain. His work included the identification of Nogo and its receptor NgR1. This pathway was shown to play a role in limiting recovery after spinal cord injury and stroke. A key focus now is the study of brain plasticity and its modulation by NgR1 and by injury. Technically, he utilizes chronic in vivo imaging of neuronal connections, genetic alteration of mice and induction of surgical lesions resembling clinical trauma and stroke. More recently, Dr. Strittmatter has focused on pathophysiological ligand–receptor pairs in the degenerative dementias. Molecular contributions of particular ligands for these pathologies had been discovered by genetic methods, but their mechanism of action remained poorly understood. Dr. Strittmatter has focused on defining the pathophysiological action of Amyloid-beta (Aβ) peptide oligomers in Alzheimer's disease, and on the role of secreted Progranulin in Fronto-Temporal Lobar Degeneration. For both of these molecules, interaction with the specific receptors on the neuronal surface is crucial. His investigations have led recently to the identification of PrPC and Sortilin as sites for Aß and PGRN, respectively. He has defined a molecular pathway from Aßo through PrPC to mGluR5 and Fyn kinase leading to synaptic dysfunction in AD models. His laboratory utilizes receptor ligand binding assays, expression cloning, electrophysiology, genetics and mouse behavior to study these pathways.