Buckwalter Lab:
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.
Andreasson Lab:
We are interested in understanding the mechanisms by which neuroinflammation elicits synaptic and neuronal injury in chronic and acute models of neurological disease. Our foot in the door has been the study of the cyclooxygenase-2 (COX-2) pathway and its downstream prostaglandin receptor signaling pathways, which function in important ways in modulating the inflammatory response in brain in models of Alzheimer's disease (AD), amyotrophic lateral sclerosis (ALS), Parkinson's disease (PD), and stroke. Thus this pathway functions across a broad spectrum of neurodegenerative diseases, and may potentially modulate inflammatory responses and neuronal injury via conserved cellular and molecular mechanisms. We use genetic and pharmacologic strategies as well as in vitro culture approaches to define COX-2/prostaglandin receptor mediated mechanisms of action in eliciting synaptic and neuronal injury in models of human neurological disease. Our long-term goal is to (1) further understand how neuroinflammatory processes injure synapses and neurons and disrupt circuits, (2) define the contribution of the COX-2/prostaglandin signaling pathways in this process, and (3) develop therapeutic strategies targeting injurious inflammatory processes in human neurological diseases.
Neurosurgical labs: http://neurosurgery.stanford.edu/research/labs.html
Neurology labs: http://neurology.stanford.edu/labs/researchlabs.html
