Scientists have published a proof-of-concept study in the journal Neurobiology of Disease demonstrating that an antidepressant drug which has been on the market for more than 50 years could slow the progression of Parkinson’s.

The drug nortriptyline, which has been used to treat depression and nerve pain, stopped the growth of abnormal proteins that can build up in the brain and lead to the development of the disease.

Researchers began by examining previous patient data to see if individuals who were on antidepressants started a standard Parkinson’s therapy called levodopa later than those not taking the antidepressant. Levodopa increases levels of dopamine, a natural chemical in the body that sends signals to other nerve cells, which is usually significantly decreased in people with Parkinson’s. The medication also alleviates symptoms of the disease such as tremors and poor muscle control.

The researchers observed that people on tricyclic antidepressants did not need levodopa until much later, compared to patients not taking a tricyclic for depression.

Researchers then began testing rats with the tricyclic antidepressant nortriptyline and observed that it decreased the amount of alpha-synuclein, an abnormal protein that can build up in the brain and cause nerve cells to die. Alpha-synuclein buildup is a hallmark of Parkinson’s diease.

Finally, the scientists added nortriptyline to alpha-synuclein proteins in a test tube model and observed that the addition of the antidepressant caused the proteins to move and change shape more rapidly, preventing them from clumping together.

To further back up his research, he enlisted the help of his colleague and co-author Lisa Lapidus, who in previous studies had already detected whether certain compounds could bind to alpha-synuclein and stop it from accumulating.

Understanding how these proteins can clump together could point researchers in new directions and help them find other possible drugs that could potentially treat Parkinson’s.

Paper: “Nortriptyline inhibits aggregation and neurotoxicity of alpha-synuclein by enhancing reconfiguration of the monomeric form

Reprinted from materials provided by Michigan State University.