Buckwalter Lab Team

Marion Buckwalter, MD, PhD

Principal Investigator
Associate Professor of Neurology and Neurological Sciences, and Neurosurgery

Dr. Buckwalter is a stroke clinician and basic scientist, and her laboratory focuses on how inflammation after stroke affects outcomes. They utilize complementary mouse models of stroke, and use transgenic, viral, and pharmacological techniques to alter inflammatory gene expression and assess the effect on outcome.

Her lab also utilizes human samples from ongoing clinical studies at the Stanford Stroke Center. Dr Buckwalter co-leads SCAN, the Stroke Collaborative Action Network, a group of Stanford researchers sponsored by the Stanford Neuroscience Institute's Big Ideas initiative to study stroke recovery.

Todd Peterson, PhD

After receiving my Bachelors (2006) and Masters (2010) degrees at the University of Wisconsin – Milwaukee, I obtained my PhD at Southern Illinois University in 2013. My current research focuses on the central nervous systems response to insult.

I am interested in understanding the complex cellular and molecular interactions that comprise the neuroinflammatory response to neural injury in an effort to develop therapeutic treatment options that produce the most optimal response to multiple types of neural insult and other neurobiological disorders. The World Health Organization reports that neurological disorders are one of the greatest threats to public health. Of the hundreds of these disorders, some of the most common are traumatic brain injury, stroke, and degenerative disorders. Although these disorders are initiated through different causes, the common underlying factor in all of these neurodegenerative diseases is neuroinflammation. The acute response is characterized by glial cell activation, oxidative stress, and edema, all of which lead to increased tissue damage. Chronic neuroinflammation is a sustained, self-perpetuating response that persists long after the onset of neural insult. There is a complex interaction between resident immune cells like microglia and astrocytes and infiltrating immune cells including neutrophils, macrophages, and T lymphocytes. This complicated response to neural injury is a defense mechanism to remove harmful agents and promote recovery, but when over active, it can contribute to further damage. My current objective is to identify the underlying mechanisms of the neuroinflammatory response in multiple different animal models of injury and neurobiological disorders. Ultimately my goal is to steer a group that is running preclinical trials on cellular and molecular compounds designed to reduce the harmful features of the neuroinflammatory response but to harness the beneficial aspects.


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