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Vasogen Preclinical Research Published in the Journal of Biological Chemistry Toronto, Ontario - March 29, 2005 Vasogen Inc. (NASDAQ:VSGN; TSX:VAS), a leader in the research and development of immune modulation therapies targeting the chronic inflammation underlying cardiovascular and neurological disorders, today announced the publication of preclinical findings demonstrating the ability of VP015, a formulation from its VP series of drugs, to significantly reverse a measure of the impairment of memory and learning function associated with aging. The data also showed that the effects of VP015 cross the blood-brain barrier and provide a neuro-protective effect against inflammation within the brain. The results, which are based on research conducted at the Department of Physiology of Trinity College in Dublin, Ireland, have been published in the Journal of Biological Chemistry in an article describing the role of the cytokine IL-4 in the regulation of age-related inflammatory changes in the brain and the action of VP015 to increase this anti-inflammatory factor. “The published preclinical data demonstrate the ability of VP015 to mediate inflammatory activity across the blood-brain barrier and to reverse a well recognized measure of neural-deficit brought on by the aging process,” stated Dr. Anthony Bolton, Vasogen’s Chief Scientific Officer. “This publication highlights the importance of IL-4 in the regulation of IL-1beta, a key inflammatory cytokine associated with inflammatory events within the brain compartment. The ability of VP015 to enhance IL-4 and IL-4 signaling activity in the brain supports the potential of VP015 to treat neurodegenerative disorders associated with inflammation.” The published preclinical data demonstrate that both the natural aging process and the administration of an inflammatory stimulus (lipopolysaccharide [LPS]) reduced concentrations of the regulatory cytokine IL-4 and the activity of the IL-4 signaling pathway in the hippocampus of the brain. There was a concomitant increase in levels of the pro-inflammatory cytokine interleukin-1beta (IL-1beta) and activity of the IL-1beta signaling pathway. The administration of VP015 significantly enhanced IL-4 levels (p<0.05) and was associated with a reduction in IL-1beta levels (p<0.05), demonstrating the anti-inflammatory effect of VP015 in these models. The persistent enhancement of the synaptic response in a specific neural pathway in the hippocampus is described by long-term potentiation (LTP) and is considered to be a key physiological mechanism involved in memory and learning. The loss of the ability to sustain LTP in both aged and LPS-treated animals correlates with the increase in IL-1beta seen in these animals. The published data demonstrate that VP015 potently abrogates the reduction of this correlate of memory and learning (p<0.001), and this is associated with the change in the balance of anti-inflammatory IL-4 and pro-inflammatory IL-1beta measured in the brains in these animal models. VP015 is one of a series of structurally related drugs that are designed to interact with immune cells leading to the modulation of cytokines – potent chemical messengers that regulate and control inflammation. VP025, the lead product candidate from this new class of drugs, is being developed for the treatment of certain chronic neurological disorders. Neurological conditions that are associated with an inflammatory response in the brain and central nervous system include Alzheimer’s disease, Parkinson’s disease, ALS (Lou Gehrig’s disease) and multiple sclerosis. These indications 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.
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