Pain is a protective mechanism but chronic pain can be life-threatening. It leads to long-term changes throughout the nervous system called 'neuroplasticity'. The immune system is also a defense mechanism and interaction between the nervous and the immune systems influences the intensity and duration of pain secondary to nerve damage. The challenge is to better understand this interaction and to propose approaches that would help in reversing neuroplasticity and consequently chronic pain.

Biography

Carl Saab is a PhD Neuroscientist studying nervous system diseases. He obtained his PhD in 2001 from the University of Texas Medical Branch in the field of pain research mapping pain pathways in the cerebellum (thesis advisor WD Willis). He then completed his postdoctoral fellowship in the laboratory of Stephen Waxman at Yale studying sodium channelopathies in pain and multiple sclerosis. Currently Carl is Assistant Professor at Brown University & Rhode Island Hospital, Neurosurgery and Neuroscience.

Research Description

Pain is a national health problem with over $150 billion/year in direct costs and lost productivity. Hospitalized patients with intractable pain experience increased length of stay, longer recovery time and weakened immunity. Normally the nervous system and the immune system are protective mechanisms. However, certain diseases that damage nerves such as diabetic neuropathy and viral infections, or following trauma, interaction between immune cells and neurons may lead to intractable pain that is life-threatening by itself.
In the laboratory, I study immune cells in the spinal cord and the brain called 'glia' to identify molecular signaling pathways that sensitize 'pain neurons'. I also study the phenomenon of long-term changes in the nervous system called neuroplasticity that is caused by chronic pain. Currently investigated methods to reverse neuroplasticity include direct brain intervention using pharmacological (analgesic small peptides, glial inhibitors, receptor blockers), technological (deep brain stimulation) and stem cell transplant approaches. I am part of a larger team within the department of neurosurgery that focuses mainly on translational research in the areas of pain, Alzheimer, Parkinson and stroke.

Awards

Ambassador Award, 2010 Executive Mentorship Program at Lifespan January 4 2011

Speaker at the 2010 Executive Mentorship Program Ceremony January 4 2011

2010 Executive Mentorship Program Mar-Dec 2010
(Mentoring with Bradley Hospital CEO, Dan Wall)

Who's Who in Medicine Higher Education April 22 2010

Finalist for RIH Research Celebration New Investigator Award Oct 22 2009

Travel award, Baltic Summer School, Kiel, Germany August 16-30 2003

Young Investigator Travel Support, American Pain Society (APS) April 19-22 2001
20th Annual Scientific Meeting, Phoenix, Arizona
Young Investigator Travel Support and Citation Poster awards, APS November 2-5 2000
19th Annual Scientific Meeting, Atlanta, Georgia

Travel award, International Society for Magnetic Resonance in Medicine May 1999
7th meeting, Philadelphia, Pennsylvania

Travel award, International Association for the Study of Pain August 1999
9th World Congress on Pain, Vienna, Austria

Travel award, University of Wisconsin 1999
Symposium on Health and Emotion, Madison, Wisconsin

Travel award, University of Wisconsin 1998
Symposium on Health and Emotion, Madison, Wisconsin

Certificate of Achievement in Teaching, UTMB Spring 1998
Physiology, Allied Health School

Who's Who Among Students In American Universities & Colleges (# 11 187-24-0-99) 1998

Scholarship (40% Tuition), AUB 1992- 1994

Affiliations

Visiting Lecturer, American University of Beirut, Lebanon, 2-14/3-10 2004; 1-27/2-12 2006.

Funded Research

Rhode Island Foundation Jan 2006
"Mechanisms of Neutrophil Recruitment to Dorsal Root Ganglia after Nerve Injury"

NIH, R01NS055251 (PI Diane Lipscombe) 2006 - 2010
"N-type Calcium Channels in Nociceptive Neurons"

Stryker Dev. April 2006
"Vagal Nerve Stimulation"

NIH, R21NS061176 (PI John Marshall) 2008 - 2010
"Development of Neuroprotective PDZ-domain Inhibitors for the Treatment of MS"


NIH, R21DK081628 (PI Elie Al-Chaer) 2008 - 2010
"Mechanisms of Microglia in Visceral Pain"

NIH, R21DK081845 (PI Saab) 2010 - 2012
"Spinal Microglial Mechanisms of Visceral Hypersensitivity"

Teaching Experience

Lecturer (6-hrs), Brown, Neuroscience (BN205): Advanced Systems Neuroscience, Neuroscience, December 30, January 1/7/8 2005.

Courses Taught

• Advanced Systems Neuroscience (BN0205)
• Advanced Systems Neuroscience (BN205)

View My Full Publication List in pdf format

Selected Publications

• 1. LeBlanc B.W., Iwata M., Mallon A.P., Rupasinghe C.N., Goebel D.J., Marshall J., Spaller M.R., Saab C.Y. A Cyclic Peptide Targeted against PSD-95 blocks central sensitization and attenuates thermal hyperalgesia. Neurosci 167:490-500, 2010.(2010)
• 2. Saab C.Y. and Hains B.C. Remote neuroimmune signaling: a long-range mechanism of nociceptive network plasticity. TINS 32:110-7, 2009.(2009)
• 3. Shaw S.K., Owolabi S.A., Bagley J., Morin N., Cheng E., LeBlanc B.W., Kim M., Harty P., Waxman S.G. and Saab C.Y. Activated polymorphonuclear cells promote injury and excitability of dorsal root ganglia neurons. Exp Neurol 210(2):286-94, 2008 (COVER).(2008)
• 4. Saab C.Y., Wang J., Gu C., Garner K.N. and Al-Chaer E.D. Microglia: A newly discovered role in visceral hypersensitivity. Neuron Glia Biol 2:1-7, 2007.(2007)
• 7. Hains B.C., Saab C.Y. and Waxman S.G. Alterations in burst firing of thalamic VPL neurons and reversal by Nav1.3 antisense after spinal cord injury. J Neurophysiol 95:3343-3352, 2006.(2006)
• 5. Black J.A., Liu S., Hains B.C., Saab C.Y. and Waxman S.G. Long-term neuroprotection of central axons with phenytoin in monophasic and chronic-relapsing murine EAE. Brain 129:3196-208, 2006.(2006)
• 6. Owolabi S.A. and Saab C.Y. Fractalkine and minocycline alter neuronal activity in the spinal cord dorsal horn. FEBS Lett 580:4306-10, 2006.(2006)
• 8. Hains B.C.*, Saab C.Y.* and Waxman S.G. Changes in electrophysiologic properties and sodium channel Nav1.3 expression in thalamic neurons after spinal cord injury. Brain 128: 2359-71, 2005 (* equal contribution).(2005)
• 9. Hains B.C., Saab C.Y., Klein J.P., Craner M.J., Black J.A. and Waxman S.G. Altered sodium channel expression in second-order spinal sensory neurons contributes to pain after peripheral nerve injury. J Neurosci 24: 4832-4839, 2004.(2004)
• 10. Lo A.C., Saab C.Y., Black J.O. and Waxman S.G. Phenytoin protects spinal cord axons and preserves neurological function in experimental allergic encephalomyelitis. J Neurophysiol 90: 3566-3571, 2003.(2003)