Accession Number : AD1007017

Title :   Role of Adenosine Receptor A2A in Traumatic Optic Neuropathies (Addendum)

Descriptive Note : Technical Report,01 Dec 2014,31 Dec 2015

Corporate Author : Georgia Health Sciences University Augusta United States

Personal Author(s) : Liou,Gregory I ; Ahmad,Saif ; Naime,Mohammad ; Fatteh,Nadeem ; Khan,Sohail

Full Text :

Report Date : 01 Mar 2016

Pagination or Media Count : 37

Abstract : This report summarizes the research progress and outcome of Traumatic optic neuropathy (TON). The report describes that TON as a vision-threatening complication in head injury in the war. Our goal is to develop an early therapeutic intervention before the progression of TON becomes irreversible. To achieve this goal, we tested the hypothesis that increase in the extracellular levels of adenosine can offer such an intervention. Under the stress of TON, extracellular levels of adenosine increase due to its increased formation by ecto-5-nucleotidase or decreased metabolism by the intracellular adenosine kinase. Extracellular adenosine is then increased through equilibrative nucleoside transporter and activates an endogenous anti-inflammation through a receptor-mediated pathway. This lab is currently engaged in the discovery of an adenosine kinase inhibitor, which can be used to inhibit TON-induced tissue damage.


Distribution Statement : APPROVED FOR PUBLIC RELEASE