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 demonstrate that VP025 both prevented microglial activation and preserved memory and learning function during chronic infusions of beta-amyloid.
Many neurological conditions are associated with an inflammatory response in the nervous system, including Alzheimer’s disease, Parkinson’s disease, and 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.
“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.