A new Northwestern Medicine study challenges a common belief in what triggers Parkinson's disease.
Degeneration of dopaminergic neurons is widely accepted as the first event that leads to Parkinson's. But the new study suggests that a dysfunction in the neuron's synapses -; the tiny gap across which a neuron can send an impulse to another neuron -; leads to deficits in dopamine and precedes the neurodegeneration.
We showed that dopaminergic synapses become dysfunctional before neuronal death occurs. Based on these findings, we hypothesize that targeting dysfunctional synapses before the neurons are degenerated may represent a better therapeutic strategy." Northwestern scientists found that dopaminergic synapses are not functioning correctly in various genetic forms of Parkinson's disease. This work, together with other recent studies by Krainc's lab, addresses one of the major gaps in the field: how different genes linked to Parkinson's lead to degeneration of human dopaminergic neurons.
The story of two sisters whose disease helped advance Parkinson's research Two sisters had the misfortune of being born without the PINK1 gene, because their parents were each missing a copy of the critical gene. This put the sisters at high risk for Parkinson's disease, but one sister was diagnosed at age 16, while the other was not diagnosed until she was 48.
As a result, the scientists realized that Parkin has another important job that had previously been unknown. The gene also functions in a different pathway in the synaptic terminal -; unrelated to its recycling work-; where it controls dopamine release. With this new understanding of what went wrong for the sister, Northwestern scientists saw a new opportunity to boost Parkin and the potential to prevent the degeneration of dopamine neurons.
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