The Role of CD33 in the Pathology of Alzheimer's Disease
Professor Elizabeth Ehrenfeld
Alzheimer’s disease, genetic markers
Alzheimer’s is the most prevalent neurodegenerative disease in the aging population, as well as a very common cause of dementia. It is estimated that 30 million people worldwide currently have Alzheimer’s disease. This literature review poster will attempt to explain the role of CD33 in the maintenance of amyloid beta plaques and it will address the proposal that a reduction in the level of CD33 expression can be a possible treatment for the progression and presence of Alzheimer’s disease. In Alzheimer’s disease individuals have higher levels of CD33 and develop amyloid beta plaques, a pathological trademark of Late Onset Alzheimer’s disease and Familial Alzheimer’s disease. Exploring CD33’s role in amyloid plaque persistence may lead to a possible solution for the formation of amyloid plaques in Alzheimer’s patients, and as a result decrease the lethality of this disease. Resent research has suggested that CD33, a 67-KDA transmembrane glycoprotein, may contribute to the presence of amyloid beta plaques in the brain by interfering with the body’s ability clear away amyloid beta 42 (AB42) in microglial cells. Researchers have found that an allele of CD33 called SNP rs3865444 has been associated with a reduction in CD33 expression and therefore AB42.
Hutcherson, Megan, "The Role of CD33 in the Pathology of Alzheimer's Disease" (2014). Thinking Matters Symposium Archive. 34.