Marion S. Buckwalter

Clinical Focus

• Neurology

Professional Education

Postdoctoral Advisees

Kristian Doyle , Kereshmeh Taravosh-Lahn

Graduate & Fellowship Program Affiliations

• Neurology and Neurol Sciences
• Neurosciences
• Neurosurgery

Web Site Links

• Buckwalter Lab Site

Research Interests

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...

Clinical Trials

• Diagnostic Utility of MRI in Intracerebral Hemorrhage Recruiting
• Minimally Invasive Surgery Plus rt-PA for ICH Evacuation (MISTIE) Recruiting

Publications

• Glia-dependent TGF-beta signaling, acting independently of the TH17 pathway, is critical for initiation of murine autoimmune encephalomyelitis. Luo J, Ho PP, Buckwalter MS, Hsu T, Lee LY, Zhang H, Kim DK, Kim SJ, Gambhir SS, Steinman L, Wyss-Coray T. J Clin Invest. 2007; 117 (11): 3306-15
• Chronically increased transforming growth factor-beta1 strongly inhibits hippocampal neurogenesis in aged mice. Buckwalter MS, Yamane M, Coleman BS, Ormerod BK, Chin JT, Palmer T, Wyss-Coray T. Am J Pathol. 2006; 169 (1): 154-64
• Increased T cell recruitment to the CNS after amyloid beta 1-42 immunization in Alzheimer's mice overproducing transforming growth factor-beta 1. Buckwalter MS, Coleman BS, Buttini M, Barbour R, Schenk D, Games D, Seubert P, Wyss-Coray T. J Neurosci. 2006; 26 (44): 11437-41
• Modelling neuroinflammatory phenotypes in vivo. Buckwalter MS, Wyss-Coray T. J Neuroinflammation. 2004; 1 (1): 10
• Construction of a 3-Mb contig and partial transcript map of the central region of mouse chromosome 11. Watkins-Chow DE, Douglas KR, Buckwalter MS, Probst FJ, Camper SA. Genomics. 1997; 45 (1): 147-57