Discovery Could Help Find Alzheimer’s Cure

Scientists from MGH have pinpointed a protein that they think leads to Alzheimer's.


Brain photo via Shutterstock

In February, we reported on research that says rates of Alzheimer’s disease will triple in the next 40 years. It’s scary stuff, but a new discovery from Massachusetts General Hospital could shed new light on how to treat the debilitating disease.

Dr. Rudolph Tanzi, a neurogeneticist from MGH, and his team found that an excess of the protein CD33 in the brain prevents a protein called beta-amyloid from being removed from the brain, causing a build up of plaque that eventually leads to Alzheimer’s. Tanzi says in a report from the National Institute of Mental Health (NIMH):

“Too much CD33 appears to promote late onset Alzheimer’s by preventing support cells from clearing out beta-amyloid containing plaques,” said Tanzi in a release issued by NIMH. The same release quotes Thomas R. Insel, M.D., Director of NIMH, as saying, “These results reveal, for the first time, a potentially powerful mechanism for protecting neurons from damaging toxicity and inflammation in brain disorders.”

The researchers also found that levels of CD33 were especially high in microglial cells, a type cell responsible for clearing out waste and dangerous substances—including beta-amyloid— from the brain, leading them to believe that CD33 impaired their ability to function properly. They backed up that hypothesis further by turning off the CD33 gene in mice, which caused a drop in beta-amyloid and other plaques associated with Alzheimer’s.

So what this all means is that if scientists can pinpoint a way to target the CD33 gene when developing pharmaceuticals, they may be able to stop or slow the onset of Alzheimer’s. The NIMH report says:

Collectively, these findings suggest that CD33 is a key mediator of beta-amyloid accumulation in the brain. The results imply that blocking CD33 would enhance the brain’s ability to clear beta-amyloid more efficiently, reducing downstream AD [Alzheimer’s Disease] pathology. Tanzi’s team is now trying to identify drugs that can inactivate CD33 as novel means for treating and preventing AD.

One other thing to keep in mind: Though the numbers and reports about Alzheimer’s can be shocking, you can do your part to make sure you don’t get it. Tanzi told us last December that protecting yourself from Alzheimer’s is largely in your control. “One of the biggest misconceptions about Alzheimer’s is that if you have a family history, you’re going to get it,” Tanzi says.“Lifestyle can make a difference regarding risk.”