About
Research
Overview
Neural Repair and Neuro-Degeneration Neurological injury frequently interrupts connections while sparing nerve cells. Spinal Cord Injury (SCI) is the epitome of a disconnection syndrome, in which surviving neural tissue fails to function due to lost communication at the level of injury. For the organism to regain function, new pathways must form by growth of cut or surviving nerve fibers. Unfortunately, the growth of axons and the rearrangement of brain circuitry are extremely limited in the adult brain and spinal cord.We focus on understanding the molecular pathways that limit fiber growth and functional rewiring of neuronal circuits during health and disease. Axonal growth encompasses both neural plasticity and repair. Technically, we utilize CRISPR-based genetic screens, single cell transcriptomic profiling, mutant mice and surgical lesions to model spinal cord injury. These activities support the development of novel therapies now in clinical testing.In Alzheimer's Disease and several other neurodegenerative conditions, nerve cells are lost over time. Molecular contributors to this pathology have been discovered by genetic methods, but their mechanism of action has remained poorly understood. We have focused on defining the pathophysiological action of Amyloid-beta (Aß) peptide oligomers in Alzheimer's Disease, and on the role of secreted Progranulin in Fronto-Temporal Dementia. For both of these molecules, interaction with the specific receptors on the neuronal surface is crucial. We utilize utilize receptor ligand binding assays, CRISPR-based genetic screens, single cell transcriptomic profiling, mutant mice, histopathology, PET imabehavior and cryo-electron microscope to define these pathways. These novel approaches are being translated to clinical trials.
Medical Research Interests
Academic Achievements & Community Involvement
Clinical Care
Overview
Stephen Strittmatter, MD, is a neurologist at Yale Medicine specializing in memory disorders, including Alzheimer’s disease and other forms of dementia. (Dementias are complicated conditions that involve changes to the connections between neurons in the brain that can affect basic human cognitive functioning.)
His interest in the brain and degenerative brain disorders originated at Johns Hopkins, where he completed his MD and PhD training. He went on to do his medical internship and Neurology residency at Massachusetts General Hospital before arriving at Yale University in 1993. Currently, Dr. Strittmatter teaches as the Vincent Coates Professor of Neurology and conducts research in the Strittmatter Lab on repair and regeneration of neurons in patients with dementia.
“Dementia and remembering who we are is really at the core of this whole problem of how the brain works and our personalities,” he says. “This disease can be the scariest thing, in the sense that we lose the essence of who we are.”
In addition to teaching and research, Dr. Strittmatter sees patients at the Memory Disorders Clinic. He spends a significant amount of time with each patient to get to know their medical history and how their condition has affected their lives. He also works closely with patients’ families, who are often heavily involved in the patient’s care.
He makes sure to take the time to explain the condition to his patients and their family members: “I hope for a good medical outcome, number one,” he says,” but I also hope that they feel as though we understand what’s going on with them and that we’ve done our best to give them a diagnosis, a prognosis, and to find the right treatment.”
Dr. Strittmatter applies the knowledge he gathers from research to help patients. “A key part of what we do in the clinic is determine which brain chemistries are affected. We may try different therapies to alleviate symptoms, and in rare cases, the root causes that are treatable,” he says.
Clinical Specialties
Fact Sheets
Alzheimer's Disease
Learn More on Yale MedicineDementia
Learn More on Yale MedicinePsychological Assessment of Children
Learn More on Yale Medicine
Board Certifications
Neurology
- Certification Organization
- AB of Psychiatry & Neurology
- Original Certification Date
- 1991
Yale Medicine News
News & Links
Media
- Oligomeric Beta-Amyloid Binding to Cultured Hippocampal Neurons.
- Raphespinal Axon Regeneration after Spinal Cord Transection in Mice Lacking Nogo Receptor.
- In a mouse model of Alzheimer's disease, amyloid beta clusters (red) build up among neurons (green) in a memory-related area of the brain.