Scientists believe that they may have discovered why long-term use of levodopa can lead to dyskinesia in Parkinson’s disease patients, a finding that could lead to new ways of treating or preventing dyskinesia. The results of this study have been published in the journal Neuron.

While other studies have evaluated the dopamine receptors that remain in the brain and become over-reactive to levodopa therapy over time, researchers from the Columbia University Medical Center instead focused on how neurons of the basal ganglia regulate movement in the absence of dopamine. The team utilized a novel form of optogenetics (using light to control neurons that have been genetically sensitized to light) and found that striatonigral neurons lose their ability to respond to the neurotransmitter GABA (gamma-aminobutyric acid) after long-term dopamine loss. It is notable that this effect was not found with short-term dopamine loss.

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“Our findings suggest that GABA and GABA receptors are still present in the striatonigral neurons,” said lead author Anders Borgkvist, PhD. “The implication is that this defect is correctable, and that would mean that we could prevent or at least delay dyskinesia, so that patients could continue to use levodopa.”

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