Alzheimer’s disease (AD) is a progressive neurodegenerative disorder that affects a large number of elderly people and causes the most common form of dementia. It has been estimated that in the U.S., there are currently about 4.5 million afflicted individuals and the number will increase to 14 million by 2050. It is characterized by progressive amyloid formation comprising the peptide Aβ1-42 and Aβ1-40, which leads to the development of senile plaques. Furthermore, surrounding the senile plaque are astrocytes expressing a calgranulin protein, S100b, which is a cytokine associated with chemoattractant activity for monocytes and activation of inflammatory cells of the myeloid lineage.
While current therapies for Alzheimer’s disease focus on improving the symptoms of the cognitive dysfunction, much research is being dedicated to identifying new disease modifying approaches. These approaches range in scope from inhibiting the formation of Aβ1-42 by inhibiting the enzymatic post-translational processing of amyloid precursor protein (APP) to the generation of vaccines that result in the removal of Aβ1-42 from circulation as well as the reduction of Aβ plaques.