Johns Hopkins Researchers Identify New Biological Target for Stopping Parkinson

Johns Hopkins Medicine study finds targeting the Aplp1 and Lag3 interaction could slow the progression of Parkinson’s and potentially treat other neurodegenerative diseases.
Johns Hopkins Medicine researchers have discovered a new potential biological target for halting the spread of Parkinson’s disease-causing alpha-synuclein in studies with genetically engineered mice. They have identified Aplp1, a cell surface protein, as a key player in this process.

The findings, published May 31 in Nature Communications, reveal how Aplp1 connects with Lag3, another cell surface receptor, in a key part of a process that helps spread harmful alpha-synuclein proteins to brain cells. Those protein buildups are hallmarks of Parkinson’s disease.

Notably, the researchers say, Lag3 is already the target of a combination cancer drug approved by the U.S. Food and Drug Administration (FDA) that uses antibodies to “teach” the human immune system what to seek and destroy.