srt2@case.edu
Stroke is the third leading cause of death and the leading cause of disability in the US . It is expected that the incidence of stroke will increase as the population ages. New therapies are desperately needed to limit the consequences of stroke. We have been examining the role of peroxisome proliferator-activated receptor- g (PPAR g ) in ischemic stroke. We find that Thiazolidinediones, PPAR g agonists, already in clinical use for the treatment of type-2 diabetes, reduce infarction size dramatically. This protection is associated with reduced inflammation and this is the likely mechanism of protection. We are examining the mechanisms of reduced inflammation and neuroprotection and also conducting experiments aimed at extending the time window of efficacy for Thiazolidinediones after the onset of cerebral ischemia.
Publications:
Sundararajan, S , and G. E. Landreth (2004). Anti-inflammatory properties of PPAR g agonists following transient focal ischemia. Drug News and Perspectives 17: 229-36.
Sundararajan, S. , J Gamboa, N. Victor, E. Wanderi, W.D. Lust and G.E. Landreth (2005). Peroxisome proliferator-activated receptor- g ligands reduce inflammation and infarction size in transient focal ischemia. Neuroscience, 130: 685-696. 
PPARg-IR neuron in ischemic brain |
