Esther Shohami, PhD received her doctorate in Physiology from the Hebrew University (HU), Jerusalem, Israel and did her post-doc at MC-Gill University in Montreal, Canada. She later joined the HU School of Pharmacy at the faculty of medicine and is currently a Professor Emerita in Pharmacology at the HU Institute for Drug Research. Between 2006 - 2011 she served as the Dean of students at her University, and between 2012-2014 as the president of the Israel Society for Neuroscience. She is a member of the executive board of the International Neurotrauma Society (INTS) and serves on the editorial boards of J. Neurotrauma. She also served as a council member of the US National Neurotrauma Society and on the editorial board of J. CBF & M.

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Prof. Shohami has published more than 220 articles, reviews, and book chapters. Her research is focused on experimental traumatic brain injury (TBI) in rodents and addresses mechanisms of injury (e.g, inflammation, oxidative stress, the glutamate NMDAR) and endogenous neuroprotection (e.g. endocannabinoids and heat-acclimation induced preconditioning). Currently, her work focuses on the effects of TBI on cognitive functions and on mechanisms involved in ameliorating these TBI-induced deficits. She also studies the involvement of the endocannabinoid system in the pathophysiology and rehabilitation after TBI and is involved in developing cannabinoid-like novel drugs for TBI. The protective Role of Endocannabinoids in Traumatic Brain Injury.

 

Presentation Information:
This presentation is dedicated to the memory of Prof. Rafi Mechoulam, the pioneer and founding father of cannabis as a novel research field in basic and clinical science.
 

Traumatic brain injury (TBI), a major health problem with significant, worldwide socioeconomic burden affecting millions of people, is a complex, dynamic and heterogeneous pathology. To date, there is no effective treatment to this "silent epidemic." TBI triggers the accumulation of harmful mediators and results in injury cascades that evolve into chronic brain damage. However, endogenous, protective mechanisms to attenuate damage are also set in motion. In this presentation we will discuss the role the cannabinoids play to improve the outcome of TBI, in a mouse model of closed head injury.

Three types of cannabinoid-related compounds that act to reduce brain damage after TBI will be discussed:

1. The endocannabinoids (eCB) that are produced by the brain.

2. The plant-derived, non-psychotropic compound, cannabidiol (CBD)

3. Synthetic compounds, that target the CB2 receptor.

 

The endocannabinoids (eCB):
2-arachidonoylglycerol (2AG) is the main brain constituent of the endocannabinoid (eCB) system and is an agonist of the both CB 1 and CB2 receptors. The levels of 2-AG are significantly elevated in a mouse model after TBI, and the mechanisms by which it affords neuroprotection will be discussed. N-arachidonoyl-L-serine (AraS), was also identified as another endogenous brain constituent structurally-related to the eCBs family. However, as they do not bind to known CB receptors they are referred to as
eCB-like compounds. Despite its lack of affinity to CB 1 or CB 2 receptors, some of the effects of AraS are similar to those of the classical eCBs, and its mechanism of action after TBI will be discussed.
 

Cannabidiol (CBD):
CBD which is nowadays being successfully implemented in various disease therapies and will be discussed as potential tool to treat TBI. While exhibiting low activity via the CB1 and CB2 receptors, this phytocannabinoid binds to a broad spectrum of targets. When given after TBI it significantly improves short-and long-term motor and cognitive functions, accompanied by reduction of lesion volume. The diverse pathology of TBI was found to be well addressed by the multi-target cannabinoid compound, CBD.
 

Synthetic CB2 agonists:
In view of the increasing evidence that the CB 2 Receptor plays a role in the brain during neuroinflammation we tested whether selective CB 2 agonists have a beneficial effect after TBI. In mice and rats, subjected to TBI and treated with these novel synthetic compounds, we showed enhanced neurobehavioral recovery and inhibition of inflammatory mediators. We propose these CB 2 agonists as potential drugs for development of novel therapeutic modality to TBI.