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DNA shows how people with Parkinsonís may respond to treatment

July 20, 2016


Brain scientists have found genetic markers that can help predict how a person will respond to a drug used to treat symptoms of Parkinson’s disease.

“We found two genetic variants that if present in a person with Parkinson’s disease will mean a greater improvement in their symptoms during the early stages of the disease when treated with a common anti-Parkinsonian drug called rasagiline,” says Dr. Mario Masellis, lead investigator of the new study and a neurologist at Sunnybrook. “These findings could lead to customized therapy for patients.”

Parkinson’s disease (PD) is the second most common neurodegenerative disorder after Alzheimer’s, and there is no cure. “We rely on drugs that treat the symptoms to help patients manage the disease the best way possible, but the drugs don’t always work the same for everyone,” adds Masellis, also an assistant professor at University of Toronto.

With PD, the brain gradually stops producing dopamine: a neurotransmitter that helps regulate movements. People with the dopamine deficiency may experience tremors, stooping or shuffling when they walk, and have difficulties with fine motor skills like buttoning a shirt or opening a jar.

Symptoms of the disease are treated with dopamine replacement drugs or enzyme inhibitors like rasagiline, which help to block the breakdown of dopamine in the brain. But how well the drug works will vary for each person, according to previous clinical trials.

In the largest pharmacogenetic study of its kind in Parkinson’s disease conducted to date, the researchers analyzed stretches of DNA in 692 patients. They compared genetic variants with changes in Unified Parkinson’s Disease Rating Scale (UPDRS) scores, which takes into account motor symptoms, mental functioning, and mood. While the majority of the patients benefited from the drug, results showed that patients on rasagiline with the identified genetic variations experienced a significantly greater improvement in their motor and mental symptoms at 12 weeks of taking the drug compared to the placebo group and those without the genetic variations.

Masellis emphasizes more research is needed, but says that the genetic associations are encouraging. “Pharmacogenetics and, more broadly, personalized medicine are exciting avenues to pursue in PD treatment, with the intention of eventually developing clinically useful point-of-care tests that can identify responders from non-responders and those at risk of adverse drug reactions,” he says.

The study was done in collaboration with other investigators at the University of Toronto: Dr. Anthony Lang at University Health Network, and Drs. James Kennedy and Jo Knight at the Centre for Addiction and Mental Health. It was published in the July 2016 issue of the neurology journal, Brain.

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