An anti-inflammatory drug currently approved by the U.S. Food & Drug Administration to treat conditions such as ulcerative colitis and asthma delayed the onset of amyotrophic lateral sclerosis (ALS) symptoms in mice, researchers say.

Cromolyn sodium prevented motor neuron degeneration in the mice and was “neuroprotective” by decreasing inflammation, leading researchers to suspect that inflammatory processes are significantly tied to ALS.

The study, “Cromolyn Sodium Delays Disease Onset and Is Neuroprotective in the SOD1G93A Mouse Model of Amyotrophic Lateral Sclerosis,” was published in Scientific Reports in November.

In the study’s abstract, researchers said, “Accumulating evidence suggests that neuroinflammatory processes are implicated in the initiation and progression of amyotrophic lateral sclerosis.”

While neurological symptoms were delayed in all the mice that received the cromolyn sodium treatment, only female mice experienced improvement in survival rates.

“Furthermore, there was a significant increase in motor neuron survival in the lumbar spinal cord as well as a significant decrease in the denervation of the neuromuscular junction of the tibialis anterior muscle in cromolyn-treated transgenic SOD1G93A mice,” researchers said.

The 149 mice in the study, some of which had the genetic mutation that would cause ALS-like presentations, received cromolyn sodium injections once a day for five days a week. All the mice were subjected to various tests, such as the ability to fully extend their hind legs away from lateral midline when suspended by their tails. They were also observed for signs of minimal joint movement, paralysis, or the inability to stand when laid on their sides.

The mice that had been given cromolyn sodium treatments were slower to show signs of mobility impairment.