New Study Reveals Parkinson’s Disease May Be Triggered Earlier Than Previously Thought
A new study conducted by researchers from the US and Canada has shed light on the early triggers of Parkinson’s disease. The findings suggest that the condition may be initiated before previously identified symptoms manifest.
Analyzing neurons from patients with Parkinson’s disease, the researchers discovered a previously unknown culprit for the disease’s symptoms, which may start before any other triggers. This trigger is a malfunction in the synapses, or connections, between neurons that regulate dopamine production. This malfunction leads to a toxic buildup of dopamine, resulting in damage to the dopaminergic neurons that define Parkinson’s disease.
“We showed that dopaminergic synapses become dysfunctional before neuronal death occurs,” explains neuroscientist Dimitri Krainc from Northwestern University in the US. “Based on these findings, we hypothesize that targeting dysfunctional synapses before neuron degeneration may represent a better therapeutic strategy.”
The generally accepted consensus has been that problems in mitophagy, the process of recycling worn-out mitochondria in the brain, cause neuron loss and subsequent Parkinson’s symptoms like trembling. The study adds to this understanding by highlighting mutations in the Parkin gene as a cause of synapse dysfunction. This mechanism had not been previously identified and appears to be the earliest indicator of Parkinson’s disease development.
The research also provides insights into how Parkin and another gene called PINK1 operate independently of each other. Neurons from two sisters with Parkinson’s disease were included in the samples. While both sisters were born without the PINK1 gene, only one of them completely lacked the Parkin gene, leading to the puzzling diagnosis. “There must be a complete loss of Parkin to cause Parkinson’s disease,” says Krainc. “So, why did the sister with only a partial loss of Parkin get the disease more than 30 years earlier?”
The mystery was explained by the previously unknown function of Parkin in controlling dopamine release through synapses, in addition to its role in neuron recycling. This discovery paves the way for potential control over this mechanism in the future.
Parkinson’s disease affects over 10 million people worldwide, with 90,000 new diagnoses in the US each year. As global populations age, these numbers are expected to rise. The identification of this new mechanism, occurring in the brain before other potential triggers, is a significant breakthrough in the ongoing search for treatments for Parkinson’s disease.
“Now, we need to develop drugs,” says Krainc, “that stimulate this pathway, correct synaptic dysfunction, and hopefully prevent neuronal degeneration in Parkinson’s.”
The research has been published in the scientific journal Neuron.