A team of researchers led by Paramita Chakrabarty, Ph.D., an assistant professor of neuroscience, and MBI Director Todd Golde, M.D., Ph.D., has identified a potential new way to use the body’s own immune system to fight the buildup of amyloid beta plaques linked with Alzheimer’s disease.
In a study published Aug. 29 in the Journal of Experimental Medicine, the team targeted immune receptors that can bind to molecules such as the amyloid beta protein, which can aggregate and form plaques in the brains of Alzheimer’s disease patients. The researchers manually took apart certain receptor molecules — in other words, they bioengineered molecules to create smaller forms of molecules that can bind to amyloid beta and remove the amyloid beta from the brain in a mouse model of Alzheimer’s disease. Thus, these molecules acted as “scavengers,” cleaning up the excess amyloid beta proteins.
Chakrabarty said it is the first time the group has bioengineered a molecule to produce a molecule that can act as a scavenger for amyloid beta.
“We hope to use this technology to fight the buildup of other similar aggregated proteins in the brain,” Chakrabarty said. “This is like a form of immunotherapy, as used in cancer and other diseases, where the body’s own defense system can be harnessed to fight off the disease.”
The research was funded by the Accelerating Medicines Partnership – Alzheimer’s Disease program at the National Institutes of Health.