A glitch in the mechanism by which cells recycle damaged components may trigger Parkinson’s disease, according to a study by scientists at the Albert Einstein College of Medicine of Yeshiva University.

According to Reuters, the U.S. team focused on a process called autophagy in which cells digest and recycle damaged molecules, including proteins, that develop as cells grow older, essentially renewing cells to keep them functioning properly.

Ana Maria Cuervo, a cell biologist who led the study, said this mechanism is also important for nerve cells in the brain where defective proteins can kill cells and cause the debilitating symptoms of Parkinson’s, such as tremors.

The finding could potentially lead to drugs to treat the symptoms but not cure the disease, which affects more than a million patients in the United States alone and is marked by the death of brain cells that produce dopamine, a neurotransmitter, or message-carrying chemical, associated with movement, Reuters said. 

Cuervo had previously shown how mutant forms of a protein called alpha-synuclein—found in a tiny percentage of Parkinson’s patients—blocked the breakdown of substances and prevented cells from clearing damaged proteins.

The study, which appeared in a recent issue of The Journal of Clinical Investigation, showed how in the majority of patients dopamine modifies normal proteins to act like the mutated ones to trigger tremors and other symptoms.

Problems in this process have also been linked with other neurodegenerative conditions such as Alzheimer’s and Huntington’s disease, though the specific mechanisms that cause problems in those conditions are different, Cuervo said.

Cuervo said a drug to fix the breakdown in Parkinson’s patients was years away because it would take researchers time to understand fully how the process worked, Reuters reported.