Prof Larry Benowitz  
Director, Department of Neurosurgery. Harvard Childrens Hospital, Boston MA

Larry Benowitz's research focuses on restoring nerve function lost as a consequence of stroke or injury. Under normal circumstances, nerve cells in the mature central nervous system (CNS: brain, spinal cord, eye) cannot re-establish their connections after injury, nor can intact cells grow new connections to compensate for those that have been lost. As a result of this, victims of traumatic injury, stroke or neurodegenerative diseases can suffer permanent and often devastating losses in movement, sensation, bodily functions, and thinking. The goals of the Benowitz lab are to discover the basic mechanisms that control the growth of nerve connections and to apply insights from this work to promote regeneration and functional recovery after CNS injury.

Senior Research Investigator at Moscow Helmholtz Research Institute of Eye Diseases (RF), scientific consultant EXSYMOL SAM, Monte Carlo (Principaute de Monaco), senior investigator, scientific consultant Bruschettini S.r.l., Genoa (Italy), Executive Director Innovative Vision Products, Inc., Delaware (USA).
Graduated from the 2nd Moscow Medical Institute (Pirogov’s), Medico-Biological Faculty as doctor-biophysicist on June 28, 1982.
1983: Young scientific researcher at Moscow Helmholtz Research Institute of Eye Diseases,
1983-1989, Scientific researcher,
1989-1998, Senior Scientific Researcher at the same Helmholtz  Institute above cited
1998- present time:  Executive Director at Innovative Vision Products, Delaware, USA

He earned a Ph.D. in Biophysics and Pathophysiology at the Moscow Helmholtz Research Institute of Eye Diseases, Moscow, Russian Federation on April 6, 1988.

Since 1992 scientific consultant EXSYMOL SAM, Monte Carlo, Principaute de Monaco.
Since 1991- senior investigator, scientific consultant Bruschettini S.r.l.
Since 1998- current time : Executive Director, Innovative Vision Products, Delaware, USA

Contributed  97 articles to professional journals; International patentee (15) in the field.
Executive Director of Chernobyl Workers Goodwill Union since 1992.
Recipient Oka Memorial Award, Yokohama, Japan, 1992 ;
Grantee International Science Foundation in 1994

Professional Interests: Lens research, Medical optics, oxidative stress, antioxidants

2006 - Rewiring the injured brain: novel growth factors, signaling pathways, and combinatorial treatment
|Damage to the central nervous system (CNS) can result in devastating and often permanent losses of sensory, motor, cognitive, and/or autonomic functions. This poor outcome is due in part to the limited capacity of the CNS to regenerate: few neurons that die are replaced, neurons that remain alive but whose axons are injured can not regrow these, and undamaged neurons do not generally form new connections to compensate for ones that have been lost. Our lab has been investigating basic mechanisms that underlie the growth of neural connections and applying insights from this work to improve functional outcome after various types of CNS injury. In the optic nerve, a CNS pathway in which injured axons normally show no capacity to regrow, activating macrophages in the eye causes the main projection neurons of the eye, the retinal ganglion cells (RGCs), to switch into an active growth state and extend lengthy axons through the optic nerve. This growth requires mannose (a normal constituent of the vitreous), an agent to elevate intracellular [cAMP], and oncomodulin, a newly discovered polypeptide growth factor that is secreted by macrophages and other cells. Oncomodulin is an atypical Ca2+-binding protein that binds to a high-affinity receptor on RGCs. If, at the same time, RGCs are transfected with a gene that renders them unresponsive to inhibitory signals associated with myelin and the glial scar, regeneration is enhanced greatly. Axon outgrowth in this and many other systems is mediated via Mst3b, a homolog of a kinase that controls budding in yeast. Mst3b can be inhibited with the purine analog 6-TG and activated with the purine nucleoside inosine. Blocking Mst3b function or expression suppresses axon growth in culture, Conversely, activating this kinase in vivo improves anatomical rewiring and functional outcome after spinal cord injury and stroke. As in the optic nerve, combined treatments to activate neurons’ growth program while counteracting inhibitory signals enhances rewiring and behavioral outcome to an even greater extent. These and related discoveries may someday enable us to improve functional outcome after CNS injury