Marion S. Buckwalter

Research/Lab website:   Buckwalter Lab Site

Our lab focuses on how inflammatory responses after brain injury affect neurological recovery. In the United States, there are 4 million people currently living with the effects of stroke, and another 4.3 million living with the effects of traumatic brain injury. Of the people who have had a stroke, many are disabled to the degree that they cannot work, and a significant proportion are unable to walk, feed themselves, or communicate with their families the way they could prior to their stroke. Despite this very high number of people who are suffering, there is a large knowledge gap regarding the mechanisms by which neurological recovery occurs, and not a single FDA-approved therapy available to help people recover. There is reason to think that such a therapy might be obtainable – we know that some people, especially younger ones, experience significant recovery after stroke. Animal studies, almost entirely done in young animals, also demonstrate significant recovery after neurological injury. Our goal is thus to better understand the mechanisms that contribute to recovery in the young, and how they are influenced by inflammatory responses. Once we understand this, we hope to be able to develop new therapies to help people’s brains repair themselves.

Current projects in the lab:

TGF-beta signaling after brain injury. To understand the role of TGF-beta signaling after brain injury, we use mouse models to manipulate and image TGF-beta signaling after stroke, viral vectors to influence TGF-beta signaling in neural progenitor cells, and small molecule therapies in a time-restricted fashion. We measure the effects on functional recovery from brain injury, the cellular and molecular immune response, and cell-specific signaling pathways.

The effect of small molecule neurotrophin agonists on functional recovery. In collaboration with the Longo lab, which has developed these compounds, we are testing whether small molecule compounds that mimic NGF and BDNF can be used to improve recovery and stimulate regenerative responses after brain injury.

Imaging and manipulating regenerative responses after brain injury. Constructing novel mouse models to allow for real-time imaging and manipulation of neurogenesis and oligodendrogenesis in mice as they recover from brain injury.

Peripheral immune responses and brain edema after stroke. In collaboration with researchers at the Stanford Stroke Center we plan to evaluate serum samples from patients with stroke. Our goal is to understand the peripheral immune mechanisms that correlate with the development of brain edema, or swelling, and determine if there are ways to predict which patients may require more aggressive treatment for their strokes.