Lynne C. Weaver
Why I Became a Scientist
While engaged in the practice of veterinary medicine in the late 1960’s I found that my opportunity to make a significant contribution to health of animals or people was limited. Having had a brief and stimulating exposure to medical research as a veterinary student, I decided to seek a position in a research laboratory. I soon was part of a team in a large (human) hospital studying the development of cardiovascular control reflexes in newborn piglets. Because I found this work fulfilling, I entered a PhD graduate program in Pharmacology to obtain the necessary research training and credentials to make medical research my career. My research career always has been focussed on understanding and ameliorating medical problems. This now is called translational research. The two aspects of my training made this a natural effort for me and my training in veterinary medicine was easily transferred to questions pertaining to human health.
We study the inflammatory response to spinal cord injury (SCI) in rats and humans, showing an extensive role for inflammation early after injury. Cells in the spinal cord and in the blood become very damaging. Our goal is to develop treatments that block the entry of destructive cells into the injured spinal cord. We have shown that novel anti-inflammatory treatments that block this entry improve neurological functions after SCI, such as the ability to walk and have better sensation and blood pressure control. This is due blockade of damaging oxidative processes and sparing of nerve fibres around the injury. We also discovered that a systemic inflammatory response to SCI damages organs such as the lungs and kidneys. Spinal cord injury is not localized but affects the entire body. We are examining mechanisms for this widespread inflammatory response and are developing ways to protect the affected organs.
Does blockade of the entry of inflammatory cells into the injured spinal cord reduce the secondary damage that occurs beginning hours to days after the injury? Does this improve the neurological outcomes after such injury?
The secondary injury caused by inflammation in the spinal cord leads to serious exacerbation of the initial injury. Limiting that response can improve the health of an injured person by improving their ability to walk, have normal sensation, have less pain, have better blood pressure control and have better bowel, bladder and sexual functions. The quality of life for people after cord injury is greatly compromised by the damage done to nerves that control functions other than walking. If our treatments succeed in improving outcomes after cord injury, they also may help with conditions after brain injury and stroke.
The inflammatory response that occurs after significant trauma to the nervous system also leads to a generalized inflammatory response affecting the entire body. This is called a systemic inflammatory response and it leads to damage to organs such as the lungs and kidneys. We are seeking to understand how the injury to the spinal cord leads to such a response in the body. We also are determining whether our anti-inflammatory treatment that improves the condition of the spinal cord will also protect the lungs and kidneys from damage.
The systemic inflammatory response after trauma to the nervous system can lead to a condition called multi-organ failure where essential organs needed for survival begin to fail. Lung failure is one of the major causes of death in the early days after cord or brain injury. It also happens after any major trauma to the body. Therefore, as we develop neuroprotective treatments, we must consider the problems of the entire body. We are developing treatments to protect the organs as well as the injured nervous system. Fortunately, our approach to protecting the injured cord also protects organs like the lungs and kidneys.
- Baccalaureate BS Michigan State University (1966)
- Doctoral DVM Michigan State University (1968)
- PhD Michigan State University (1975)
- Internship in Veterinary Medicine, Animal Medical Center, New York, NY (1968-1969)
- Research Associate, Michigan State University, Lansing, MI (1971-1973)
- Phi Zeta (1968)
- Phi Kappa Phi (1968)
- NIH Postdoctoral Fellowship (1972-1975)
- National Institutes of Health Research Career Development Award (1978-1983)
- Michigan State University Distinguished Faculty Award (1986)
- Barbara Turnbull Challenge Project for Spinal Cord Injury Research (2001)
- Director, New Emerging Team in Spinal Cord Injury, (CIHR Award) (2003-2008)
- FORE Visiting Scholar: The Miami Project to Cure Paralysis (2004-2005)
Geremia N.M., Bao F., Rosenzweig T.E., Hryciw T., Weaver L., Dekaban G.A. and Brown A. CD11d antibody treatment improves recovery in spinal cord-injured mice. J. Neurotrauma 29(3):539-550, 2012.
Bao, F., Brown, A., Omaña, V. and L.C. Weaver. The systemic inflammatory response after spinal cord injury in the rat is reduced by α4β1 integrin blockade. J. Neurotrauma 29: 1626-1637, 2012.
Mawhinney L.A., Thawer S.G., Lu W.Y., Rooijen Nv., Weaver L.C., Brown A. and Dekaban G.A. Differential detection and distribution of microglial and hematogenous macrophage populations in the injured spinal cord of lys-EGFP-ki transgenic mice. J Neuropathol Exp Neurol. 71(3):180-97, 2012.
Bao F., Shultz S., Hepburn J., Omaña V., Weaver L., Cain D.P. and Brown A. A CD11d monoclonal antibody treatment reduces tissue injury and improves neurological outcome after fluid percussion brain injury in rats. J. Neurotrauma 29(14):2375-2392, 2012.
Shultz S.R., Bao F, Weaver L.C., Cain D.P and Brown A. Treatment with an anti-CD11d integrin antibody reduces neuroinflammation and improves outcome in a rat model of repeated concussion. J. Neuroinflammation, 2013. In press