Newly-discovered trigger for Parkinson's could prevent devastating disease
A newly-discovered trigger for Parkinson's could prevent the devastating disease before it takes hold, according to a new study.
Previous to the latest study it was thought the devastating neurological condition began when dopamine neurons in the brain started to die off. But a team from Northwestern University in the US have found that damage starts much earlier, opening avenues for new therapies to stop its progression.
Parkinson’s disease is an incurable neurological disorder characterised by tremors, rigidity and slowness of movement. In the US there are 500,000 people with Parkinson's. The new study, published in the journal Neuron, claims that the first noticeable sign of the disease is a dysfunction in the dopaminergic neuron synapse.
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The new study, published in the journal Neuron, claims that the first noticeable sign of the disease is a dysfunction in the dopaminergic neuron synapse (Getty Images/DisabilityImages)The synapse is the tiny gap across which a neuron can send an impulse to another neuron. The dysfunction leads to loss of dopamine and precedes neurodegeneration. Previous to this, the first sign was a deterioration in the actual dopaminergic neuron which they now know is caused by the dysfunctional synapse.
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The team claim that if they can successfully target the synapses then they could be in a position to stop Parkinson's developing. Dr Dimitri Krainc, chair of neurology at Northwestern University Feinberg School of Medicine, said: “We showed that dopaminergic synapses become dysfunctional before neuronal death occurs.
“Based on these findings, we hypothesise that targeting dysfunctional synapses before the neurons are degenerated may represent a better therapeutic strategy.” It has been well-established that people who carry mutations in both copies of either PINK1 or Parkin genes develop Parkinson’s disease.
The breakthrough was helped by a study by Dr Krainc into two sisters born without PINK1. One developed the disease at 16, the other at 48. They discovered that the one who developed it earlier was also missing a bit of the Parkin gene. Dr Krainc said: “There must be a complete loss of Parkin to cause Parkinson’s disease. "So, why did the sister with only a partial loss of Parkin get the disease more than 30 years earlier?”
The researchers realised that Parkin has another important job that had previously been unknown, related to the synaptic terminal where it controls dopamine release. This now gives them the chance to look for drugs that boost Parkin and prevent the dysfunction of the synapse that leads to the disease.
Dr Krainc added: “We 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.”
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