Rutgers researcher finds brain connections may reorganize in Parkinson's disease

ind-limb cluster and act like a regular hind-limb neuron. The problem is that the neuron now receives hind-limb signals but maintains its original downstream communication with the fore-limb. The result is that the brain is unable to process these signals to control movement of the fore-limb.

"We saw this switching of connectivity happening throughout the basal ganglia and impacting many different body parts," said West. "In some cases these neurons would affiliate with more than one cluster, making accurate response to stimulation, such as touch, almost impossible."

According to West, this connection switching appears permanent, with these changes still evident up to a year after dopamine loss. "These switched connections may explain why L-DOPA and other drugs are unable to restore complex sensorimotor behaviors such as maintaining manual contact with an unseen moving object."

Although conducted with animal models, West's research is applicable to Parkinson's disease in humans. "Human studies of the basal ganglia show overlapping areas that control leg and arm movements organized similarly to rats, which means it is possible for connections to get switched in the human brain just as in the rat brain."

West's results are also consistent with previous studies that have shown that loss of dopamine in humans and animals causes the cortex to sprout new connections to the basal ganglia.

"These kinds of changes in connections would essentially make curing Parkinson's disease difficult or impossible," he explained.

West hopes his findings, which show apparently permanent changes caused by the loss of dopamine to the brain, will encourage more research focused not only on treating, but also preventing, Parkinson's disease.


Contact: Stacey Hersh
Rutgers, the State University of New Jersey

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