$3.2M Grant to Advance Work Into Serotonin, Its Role in Movement

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by Patricia Inácio, PhD |

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A National Institutes of Health (NIH) grant worth $3.2 million will further research into how the rewiring of serotonin-producing nerve cells — a chemical messenger mostly involved in mood, cognition and memory — might help with controlling movement in people with advanced Parkinson’s disease.

The grant, given to Christopher Bishop, PhD, a psychology professor at Binghamton University in New York, will run for five-years and support work that could lead to new treatments.

Parkinson’s is caused by the loss of neurons, or nerve cells, that produce the neurotransmitter dopamine — a chemical messenger essential for muscle control.

Seminal research from Bishop’s lab showed that the neurotransmitter serotonin also play a role in movement control in patients with mid- to late-stage disease.

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Serotonin may serve as a kind of “backup system” should dopamine-producing neurons be lost, the researchers speculate, as in healthy people it seems to play a minor role.

“Movement is such an important feature of our survival and our ability to flourish. If we lose movement, evolutionarily, we’re done,” Bishop said in a press release. “So there must be these backup systems that come into play.

“I think what we’re seeing in Parkinson’s disease is the ability of these circuits to rewire sufficiently so that they continue to foster movement and survival,” he added.

Targeting the serotonin system may have the same therapeutic benefits of L-dopa, a molecule that can be converted to dopamine in the brain considered the current gold standard treatment for Parkinson’s. But long-term use of L-dopa therapies, which include levodopa and its derivatives, often leads to dyskinesia or erratic, involuntary movements.

Prior studies have shown that serotonin-producing neurons play a central role in L-dopa-induced dyskinesia.

With this NIH grant, Bishop and his team hope to better understand precisely how L-dopa affects the brain’s capacity to restructure or rewire itself — a concept called neuroplasticity — and which includes a re-organization of the serotonin-signaling network.

“We started by looking at how drugs affected the Parkinsonian phenotype and found some really interesting effects, but didn’t understand all of the effects we were seeing,” Bishop said. “What this grant is doing is saying, ‘Let’s take a step back and use modern technologies to dissect the neuro-circuits and better understand the mechanisms that are involved in this neuroplasticity.’”

Preliminary data collected by these researchers using tissue samples from deceased patients were reported to show important clues into mechanisms at play in serotonin neuroplasticity, Bishop said. A deeper understating of these mechanisms could lead to treatments that delay or limit the risk of L-dopa side effects.