Vasogen's VP025 Prevents Detrimental Effects of Beta-amyloid

November 17, 2005
TORONTO, Nov. 17 /PRNewswire-FirstCall/ -- 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 new preclinical data presented yesterday at Neuroscience 2005, the Society for Neuroscience's 35th Annual Meeting in Washington, DC, demonstrates the ability of VP025 to prevent the detrimental neurological effects of chronic beta-amyloid exposure in a model of Alzheimer's disease."We believe that the data presented, demonstrating the ability of VP025 to preserve memory and learning function in the presence of chronic beta- amyloid exposure, provides further evidence supporting the potential of VP025 as a new treatment for Alzheimer's and other dementias," stated Dr. Anthony Bolton, Vasogen's Chief Scientific Officer. "Having successfully completed our phase I program, we look forward to moving VP025 into phase II clinical development in neuro-inflammatory disease."Beta-amyloid is the major component of the plaques found in brains of Alzheimer's disease patients and is implicated in the development and progression of this condition. Beta-amyloid has also been linked to increased activation of microglial cells (inflammatory immune cells in the brain) and reduced memory and learning function. The results presented today by Dr. Marina Lynch's team from the Trinity College Institute of Neuroscience, Dublin, Ireland, demonstrate that VP025 both prevented microglial activation and preserved memory and learning function during chronic infusions of beta-amyloid.Yesterday, Vasogen also announced that two additional presentations of preclinical data at Neuroscience 2005 demonstrated the impact of VP025 on key inflammation-signaling pathways. VP025 was shown to inhibit p38 MAP kinase, a key component of the inflammation-signaling pathway, regulating IL-1, TNF-alpha, and other immune system responses associated with many inflammatory conditions. In a separate model demonstrating the association of aging with increased inflammation in the central nervous system, VP025 was shown to increase CD200, a protein that controls inflammation and maintains microglial cells in an un-activated state.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.