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2008 | 2007 | 2006 | 2005 | 2004 | 2003 | 2002 Vasogen’s VP025 Shown to Impact Inflammation-Signaling Pathways Toronto, Ontario - November 16, 2005 Vasogen Inc. (NASDAQ:VSGN; TSX:VAS), a leader in the research and commercial development of technologies targeting chronic inflammation underlying cardiovascular and neurological disease, announced that preclinical data presented this week at Neuroscience 2005, the Society for Neuroscience’s 35th Annual Meeting in Washington, DC, demonstrates the ability of VP025 to modulate key signaling pathways associated with inflammation. “We continue to be impressed by the consistency of the anti-inflammatory effects of VP025 across a number of preclinical neurological studies,” stated Dr. Anthony Bolton, Vasogen’s Chief Scientific Officer. “The growing body of evidence demonstrating the ability of VP025 to reduce inflammation within the central nervous system, suggests therapeutic potential in a range of neurological disorders and continues to support our plans to initiate phase II development.” On Monday, Dr. Yvonne Nolan’s team from the Department of Anatomy/Neuroscience, University College, Cork, Ireland, presented new data demonstrating the ability of VP025 to inhibit increases in levels of p38 MAP kinase, a key component of the inflammation-signaling pathway, regulating IL-1beta, TNF-alpha, and other immune system responses associated with many inflammatory conditions. In a preclinical model of Parkinson’s disease, VP025 was shown to inhibit both the increase in p38 levels and the associated death of dopaminergic neurons. The death of dopaminergic neurons in this model system leads to the onset of movement abnormalities that mimic those seen in Parkinson’s disease. Today, Dr. Marina Lynch’s team from the Trinity College Institute of Neuroscience, Dublin, Ireland, presented results from a model showing the ability of VP025 to reverse age-related inflammation in the brain. The process of ageing is associated with increased inflammation in the brain resulting from activation of microglial cells, (inflammatory immune cells of the brain), as evidenced by increases in inflammatory cytokines, including IL-1beta, and a reduction in memory and learning function (measured as long-term potentiation). CD200, a protein that controls inflammation and maintains microglial cells in an unactivated state, decreases with ageing. Treatment with VP025 in this model reversed age-related decreases in CD200 levels in the brain, reduced levels of microglial cell activation, and restored memory and learning function. Many neurological conditions are associated with an inflammatory response in the nervous system, including Alzheimer’s disease, Parkinson’s disease, and ALS (also known as Lou Gehrig’s disease). These conditions are characterized by increased levels of inflammatory mediators, including cytokines, leading to the death of nerve cells and the eventual loss of functional activity. Due to the prevalence, morbidity, and mortality associated with neuro-inflammatory diseases, they represent a significant medical, social, and financial burden. About the Society for Neuroscience About Vasogen |
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