It effects approximately 5.5 million Americans and is the sixth leading cause of death in elderly individuals. The disease is caused by a plaque formation of amyloid beta (A) in the brain. Currently, there is no cure for Alzheimer’s disease however there are five FDA approved drugs to slow the progression of Alzheimer’s disease.
Research into this disease has conventionally focused on the CNS, however, several peripheral and systemic abnormalities are now understood to be linked to AD. This has led to pursuit of understanding how altercations can contribute to AD and the creation of therapies and treatments to prevent them from occurring. As, dementia carries significant implications for patients, their families, and our society, it is imperative to determine the cause and pathway of this disease. More research focused on finding and understanding what triggers the initiation of A plaque production in the brain can lead to the discovery of a treatment for this condition.
An imbalance between the production and clearance of A is an early, an often initiating, factor in Alzheimer’s disease. Previous studies focused on targeting amyloid-A formation as a hopeful treatment of Alzheimer’s disease. One study attempted to regulate amyloid beta formation via immunotherapy. Amyloid-A targeting antibodies were used to prevent the formation of amyloid beta plaques, a hallmark condition of Alzheimer’s disease. Mouse models were used to study two different antibodies against amyloid beta formation. Results indicated a decrease in A production, an increase in hyperactivity in the cortical area, and persisting neuronal dysfunction. The increase in hyperactivity indicated neuronal synchrony, a positive indication, and so, research was redirected to finding a treatment for the neuronal dysfunction. An experiment with monoclonal antibody, 3D6 and mice resulted in a decrease of A formation in the brain, also a positive indication. Research focus was then shifted again to determine whether if neuronal dysfunction could be treated prior to plaque formation, in the earlier stages of Alzheimer’s disease. Increased hyperactivity was observed upon administration of 3D6 antibody to the mice, this indicated that antibody 3D6 exhibited a pro-excitatory effect that is dependent on the over expression of APP. Results also showed that mice treated for 5 months with exhibited reduced amounts of amyloid plaque production however this amount of reduction was less than what was observed compared to treatment with 3D6. Treatment with 3D6 provided a consistent affect of reduced aggravation.
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