By Staff More than one million Americans have neuropathic pain. Wouldn’t it be a good thing if that pain could be reduced or even eliminated? Scientists at Rutgers University think that targeting brain cells that are supposed to provide immunity, but in some cases, do the opposite – the cause chronic pain that can last…
More than one million Americans have neuropathic pain. Wouldn’t it be a good thing if that pain could be reduced or even eliminated? Scientists at Rutgers University think that targeting brain cells that are supposed to provide immunity, but in some cases, do the opposite – the cause chronic pain that can last a lifetime.
“The general thought has been that these cells are supposed to be beneficial in the nervous system under normal conditions,” said Long-Jun Wu, a professor of cell biology and neuroscience at Rutgers University. “But, in fact, in those with this neuropathic pain these cells known as microglia, have proliferated and instead become toxic.”
Wu and his team discovered that chronic neuropathic pain – caused by nerve damage as a result of an injury, surgery or a debilitating disease like diabetes or cancer – could be greatly reduced in animals if the injury was treated targeting microglia within a few days. Their research on the topic has just been published in both Nature Communications and Cell Reports.
“If we can catch that window within one to five days to inhibit microglia after nerve injury, we can partially reverse the development of chronic pain,” said Wu. “If we were able to deplete the microglia cells causing the condition before nerve injury occurs, we can permanently prevent it.”
Neuropathy occurs when nerves are injured from trauma or disease, and persists even after the injured nerve has healed. It is often resistant to pain medicine.
In laboratory studies on mice, Wu and his colleagues used chemotherapy drugs to prohibit the microglia brain immune cells from proliferating. The results from their research showed that this chemotherapy drug reduced the amount of pain the mice experienced after the injury occurred.
“What needs to be done is prevent the microglia cells from multiplying in the first place,” said Wu. “It had been thought that these cells were beneficial in a normal brain, but our research discovered how these cells function under neuropathic pain condition and initiate the problem.”
According to Rutgers, scientists have studied microglia cells in relationship to neuropathic pain for the past two decades, but Rutgers is the first to pinpoint the exact role the cells have in the initiation and maintenance of the condition. Wu and his colleagues found that the proliferation of these types of cells is one of the major contributors of microglial pain.
This discovery could lead to the development of more effective painkillers with fewer side effects, he said.
“Our research raises the intriguing possibility that minimizing microglial proliferation may be a novel approach for pain control,” Wu said. “We hope this will eventually lead to more effective pain killers that will battle this devastating disease.”
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