Salk Institute researchers have helped uncover a mechanism that could help target and kill nerve cells responsible for Lou Gehrig’s Disease (ALS), a finding that could propel new treatments for the neurodegenerative disease and other conditions, including cancer and autoimmune disorders.
Dr. Greg Lemke, a neuroscientist, immunologist and Professor Emeritus at the Salk Institute for Biological Studies, and colleague Youtong Huang participated in a study published Aug. 15 in Nature Communications.
The researchers found that immune cells in the central nervous system, known as microglia, identify and destroy specific motor neurons in the spinal cords of mice with late-stage ALS, worsening the disease.
The discovery shifts attention beyond motor neurons, which have long been the primary focus of ALS research. Scientists are increasingly investigating the role of microglia, the brain and spinal cord’s resident immune cells, in driving disease progression.
ALS affects roughly 35,000 Americans, with about 5,000 new cases diagnosed each year. The disease typically targets those aged 55 to 75 and leads to the loss of motor neurons, resulting in muscle failure, paralysis and death.
While current treatments can slow progression, they do not stop or reverse the disease.
According to the Salk researchers, microglia use proteins known as TAM receptors to locate and eliminate motor neurons in ALS-afflicted mice.
In an interview with Times of San Diego, Lemke said one of the biggest challenges in ALS research is that scientists still do not know what causes most cases of the disease.
Of their scientific research, Lemke noted they’ve found that the body is “constantly
renovating tissue” while removing dead cells. “A million cells per second are dying in your
body,” Lemke said, adding their research has “discovered the system that recognizes the
dead cells and eats them up, keeping the tissues cleaned.”
Why is this significant? Because, Lemke pointed out, there might be a way therapeutically
to induce the body to “eat cells that are not good cells,” like neurons with ALS or tumor
cells with cancer.
“Scientists have modified the cell receptor system,” Lemke noted. “It’s a very complicated thing, but you can modify and adapt the system.”
Lemke said genetic engineering therapy might one day be employed to extend disease victims’ lives on the way to finding a cure.
But first, he pointed out, scientists must unravel the root cause of autoimmune diseases.
“Drug therapy currently only delays things,” Lemke said. “It doesn’t address the underlying molecular cause of the disease. That’s really where work like ours is needed.”
