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Vasogen’s VP025 Prevents Detrimental Effects of Beta-Amyloid in Preclinical Model of Cognitive Dysfunction Toronto, Ontario - October 27, 2004 Vasogen Inc. (NASDAQ:VSGN; TSX:VAS), a leader in the development of immune modulation therapies for the treatment of cardiovascular disease, today announced that data from new preclinical research in a model of cognitive dysfunction were presented at Neuroscience 2004, the Society for Neuroscience’s 34th Annual Meeting in San Diego. The results, presented by Dr. Marina Lynch’s team from the Trinity College Institute of Neuroscience, Dublin, Ireland, demonstrate the ability of Vasogen’s VP025 to reverse a key measure of memory and learning impairment in aged animals and also to prevent such impairment in animals injected with beta-amyloid, a major component of the plaques found in brains of Alzheimer’s disease patients. “The ability to reverse an established loss of memory and learning function would represent a major advance in the treatment of Alzheimer’s disease, age-related dementia, and other neurodegenerative diseases,” stated Dr. Anthony Bolton, Vasogen’s Chief Scientific Officer. “Our increasing understanding of the effects that VP025 exerts in the impaired brain gives us confidence that this drug candidate may have therapeutic potential in combating Alzheimer’s disease and other dementias associated with aging.” The persistent enhancement of the synaptic response in a specific neural pathway in the hippocampus (the area of the brain responsible for memory and learning) is described by long-term potentiation (LTP). LTP is considered to be a key physiological mechanism involved in memory and learning function that becomes impaired in both Alzheimer’s disease and with aging. This impairment is associated with activation of microglial cells (immune cells in the brain) and an increase in markers of inflammation, including interleukin-1ß (IL-1ß) and activation of c-Jun N-terminal kinase (JNK), a kinase involved in the inflammatory process. The results presented today demonstrate both the ability of VP025 to significantly reverse the impairment in LTP (memory and learning function) in aged animals and to prevent such impairment in animals injected with beta-amyloid to model Alzheimer’s disease. VP025 was also shown to reduce activation of microglial cells and to abrogate both the age-related increase in concentration of the inflammatory cytokine IL-1ß, and the activation of JNK. Additionally, VP025 was shown to modulate a key cell survival pathway involving TrkB and pERK, and also restored the age-related loss of synaptophysin, a measure of the density of neural connections (synapses) in the brain. Neurological conditions that are associated with an inflammatory response in the nervous system include Alzheimer’s disease, Parkinson’s disease, and ALS (also known as Lou Gehrig’s disease). 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. About the Society for Neuroscience About Vasogen |