Publication date: Jan 14, 2020
So far, the prevalent view among Parkinson’s disease specialists has been that the motor symptoms occur when dopaminergic neurons – the brain cells that synthesize the chemical messenger dopamine – start dying off abnormally.
Therefore, to try to offset motor symptoms, doctors may prescribe people with Parkinson’s disease a drug called levodopa (or L-DOPA), which helps boost the brain’s reserve of dopamine.
The research, which appears in the journal Current Biology, found that symptoms of Parkinson’s disease appear before the premature death of dopaminergic neurons.
They found that before the dopaminergic neurons die off, they stop functioning – that is, they stop correctly synthesizing dopamine – and this sets off the symptoms associated with Parkinson’s disease.
The researchers confirmed that this process occurs not just in animal models, but also in the brains of people with Parkinson’s disease.
But when the researchers used optogenetic tools once more, this time to restore function in the dormant dopaminergic neurons, the Parkinson’s-like symptoms decreased in severity.
“So far, it had been firmly believed that idiopathic [Parkinson’s disease] is caused by the death of dopaminergic neurons in [the] substantia nigra [a structure of the brain],” notes Jeon.
- Mechanism of the neuroprotective effect of injecting brain cells on ST36 in an animal model of Parkinson’s disease.
- Multiple neuronal circuits for variable object-action choices based on short- and long-term memories.
- A mitochondrial uncoupler prodrug protects dopaminergic neurons and improves functional outcome in a mouse model of Parkinson’s disease.