In a study co-funded by Cure Alzheimer’s Fund and the National Institutes of Mental Health, Rudy Tanzi, Ph.D., showed that excessive amounts of CD33 play a role in the development of late-onset Alzheimer’s disease. A variant of the gene CD33 impedes the clearance of amyloid beta. However, a mutation of the gene causes amyloid to be cleared more quickly and is actually protective against the disease. Tanzi first identified the gene as part of the Alzheimer’s Genome Project™, an effort started by Cure Alzheimer’s Fund in 2008 to identify all genes connected to Alzheimer’s disease.