Conventional beliefs over the events that first trigger Parkinson’s disease are being challenged by research that suggests damage occurs much earlier than was thought.
It has long been held that the onset of the brain disorder is heralded by the degeneration of “dopaminergic” neurons — those that produce the “feel-good” hormone dopamine.
The new study, however, suggests that, before this, a dysfunction in the synapses — the gaps between neurons across which these nerve cells can transmit impulses — can lead to deficits in dopamine that precede neurodegeneration.
Parkinson’s disease is estimated to affect around one–two percent of the population — and is characterised by resting tremors, rigidity, and a slowness of movement known as bradykinesia.
These motor symptoms are the result of a progressive loss of loss of dopaminergic neurons in the midbrain.
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The study was undertaken by neuroscientist Dr Dimitri Krainc of Northwestern University and his colleagues.
The researchers analysed midbrain neurons derived from human patients — an advantage over studies involving mouse models, which do not translate as mice and humans have different dopamine neurons.
Dr Krainc said: “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.”
Specifically, the team found that in various genetic forms of Parkinson’s disease, dopaminergic synapses do not function correctly.
In a press release, the team explained: “Imagine two workers in a neuronal recycling plant. It’s their job to recycle mitochondria, the energy producers of the cell, that are too old or overworked.
“If the dysfunctional mitochondria remain in the cell, they can cause cellular dysfunction. The process of recycling or removing these old mitochondria is called mitophagy.
The two workers in this recycling process are the genes Parkin and PINK1.
“In a normal situation, PINK1 activates Parkin to move the old mitochondria into the path to be recycled or disposed of.”
Previous studies have established that people who carry mutations in both copies of either PINK1 or Parkin go on to develop Parkinson’s as a result of ineffective mitophagy.
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The team’s breakthrough came by comparing two siblings that were both born without the PINK1 gene — placing them both at risk of developing Parkinson’s.
However, while one of the pair was diagnosed with the disease at 16, the other did not manifest the disease until age 48.
The team discovered that the woman diagnosed as a teen had a partial loss of Parkin — a fact which, by itself, should not cause Parkinson’s disease.
As Doctor Krainc put it: “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 team found that Parkin plays another role that had previously not been identified — it functions in a different pathway in the synaptic terminal that controls dopamine release.
This, they added, presents a new opportunity to boost Parkin and help prevent the degeneration of dopamine neurons.
The doc concluded: “We discovered a new mechanism to activate Parkin in patients’ neurons..
“Now, we need to develop drugs that stimulate this pathway, correct synaptic dysfunction and hopefully prevent neuronal degeneration in Parkinson’s.”
The full findings of the study were published in the journal Neuron.
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