Sept. 15 (UPI) — A groundbreaking study from Northwestern University reveals that the earliest indicators of Parkinson’s disease may differ from existing theories.
Published in the esteemed medical journal Neuron, the research proposes that a malfunction in neural synapses and cell function, not previously understood, could be the initial sign of Parkinson’s. This finding challenges the widely accepted belief that degeneration of dopaminergic neurons is the first event.
In a press release, the researchers state, “Degeneration of dopaminergic neurons is widely accepted as the first event that leaders 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.”
Parkinson’s disease, affecting approximately 1-2% of the population, may now be approached from a new angle, targeting the synapses as a potential treatment strategy.
Dimitri Krainc, a study author, expresses hope, saying, “Based on these findings, we hypothesize that targeting dysfunctional synapses before the neurons degenerate may represent a better therapeutic strategy.”
The researchers aspire to gain more insight into the genetic mechanisms behind neuronal degeneration.
The study reveals that people who develop Parkinson’s often have dysfunctional mitophagy, the process by which cells recycle mitochondria. The key genes involved in this recycling process, Parkin and PINK1, are affected by mutations in Parkinson’s patients.
Interestingly, the case of two sisters played a crucial role in unraveling the function of Parkin. While both sisters lacked the PINK1 gene, the sister who also had a partial deletion of Parkin developed Parkinson’s at 16, while the other sister remained unaffected until age 48.
This disparity led researchers to discover that Parkin is involved in dopamine release, a previously unknown function. The disruption of this function may play a significant role in accelerating the disease.
Krainc explains, “We have discovered a new mechanism to activate Parkin in patient neurons. Now we need to develop drugs that stimulate this pathway, correct synaptic dysfunction, and hopefully prevent neuronal degeneration in Parkinson’s.”
This groundbreaking research received support from grants provided by the National Institutes of Health.
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