International Stroke Conference Digest - February 21, 2008 - (Page 1)

New animal research suggests that PPAR-gamma agonists could play a role in stroke therapy P e r o x i s o m e P r o l i f e r at o r- a c t i vat e d receptor (PPAR)-gamma is a nuclear transcription factor that regulates insulin responsiveness in adipose cells, and PPAR-gamma agonists, such as pioglitazone, are used to treat patients with type 2 diabetes. However, new animal research suggests that PPAR-gamma may have a role in preventing neuroinflammation and that PPAR-gamma agonists might also benefit stroke patients. The role of PPAR-gamma in stroke is the subject of today’s symposium “PPAR-gamma: A New Target for Stroke?” The symposium meets from 4:00 to 5:30 p.m. in La Louisiane A/B. “PPAR-gamma is already a target for diabetes therapy, and new animal research is showing that whatever processes we thought were limited to type 2 diabetes or glucose intolerance may extend to vascular abnormalities and atherosclerosis,” said session co-moderator Jaroslaw Aronowski, MS, PhD, Associate Professor of Neurology and Director of Stroke Research at the University of Texas-Houston Medical School. “The processes controlled by PPAR-gamma occur on the molecular level, including regulation of phagocytosis, which could be useful in clearing the brain following any type of damage. In our lab, we have determined that by treating microglia in the brain, we can amplify the phagocytosis of red blood cells,” Dr. Aronowski explained. “For instance, in a situation of intracerebral hemorrhage or hemorrhagic transformation after an insult, you could amplify the cleaning of red blood-cell debris in the brain by activating microglia or microphages with PPAR-gamma agonists,” he said. “In addition, there are data suggesting that PPAR-gamma may play an important role at the level of neurons, so that neurons activated by PPAR-gamma agonists are made more resistant to insults that resemble insults produced by stroke; that is, oxygen glucose deprivation, and by excitotoxins released by the brain during stroke, such as glutamate,” Dr. Aronowski noted. “Furthermore, it appears that a portion of the anti-inflammatory effect of PPAR-gamma agonists could be beneficial in sustaining perfusion to the ischemic brain,” he continued. “With reperfusion after stroke, the occluded vessel opens. But in a short time, a secondary occlusion may occur due to vessel inflammation triggered by ischemia. By preventing inflammatory responses, PPAR-gamma agonists can potentially add benefit by preventing the secondary occlusion.” During the symposium, Dr. Aronowski will present a lecture titled “PPAR-gamma and Neuroinflammation” describing his research. “We have generated animals deficient in PPAR-gamma in neurons and microglia. We have evidence that the animals that do not have this transcription factor are more sensitive to damage produced by ischemia, indicating that the presence or activity of PPAR-gamma in those cells is beneficial to the system,” Dr. Aronowski said. This evidence suggests that the treatment of stroke with PPAR-gamma agonists may help neurons to survive better and stroke therapy continued on page 8 Jaroslaw Aronowski, MS, PhD Session will provide state-of-the-art update on vasospasm and neuroprotection Va s o s pa s m r e m a i n s a major cause of postoperative morbidity and mortality after subarachnoid hemorrhage. However, new therapies are being developed and studied to help protect the brain from this potentially deadly complication. Today in a session titled “Vasospasm and Neuroprotection,” four experts will discuss the current state of affairs in research, prevention, and treatment of vasospasm and its consequences. The session will meet from 7:30 to 9:00 a.m. in Room RO-6 on Level 2 of the convention center. “Beyond aneurysm re-hemorrhage, vasospasm is the next thing in line for being the major source of death and disability in patients after aneurysmal subarachnoid hemorrhage,” said session moderator Sepideh AminHanjani, MD, Assistant Professor of Neurosurgery and Co-Director of the Neurovascular Section at the University of Illinois at Chicago. “Current therapies are not as effective as we would like. Patients still suffer strokes and have significant disabilities related to refractory vasospasm. The real hope for the future is for treatments that will prevent vasospasm from occurring, whereas our current strategy is often toward treating it once it has occurred,” Dr. Hanjani said. “A lot of effort is currently directed at trials to find drugs or medical therapies that can be given to prevent vasospasm from developing, which is the ultimate goal. In the interim, we are left with patients who are still developing vasospasm, depending on the severity of their hemorrhage, at a fairly high rate and need intervention,” she explained. Vasospasm continued on page 8 http://www.strokeconference.org http://www.strokeconference.org

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International Stroke Conference Digest - February 21, 2008

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