Feinstein researcher discovers genes that repair spinal cord in fish are also in humans

Feinstein Institute researcher Ona Bloom is one of the scientists published Jan. 16 in "Scientific Reports" that many of the genes that repair an injured spinal cord in a fish called the lamprey are also active in the repair of the peripheral nervous system in mammals. (Photo courtesy of Northwell Health)

A Feinstein Institute for Medical Research scientist has helped discover that genes in a specific fish that can regenerate its spinal cord after an injury are also present in humans.

Ona Bloom, who joined the Northwell Health research institute in Manhasset in 2008, was an author of a paper published on Jan. 16 in Scientific Reports alongside her research partner Jennifer Morgan at the Marine Biological Laboratory in Woods Hole, Massachusetts.

“When I started my own lab, I wanted to work on an important clinical problem that would put both aspects of my training to good use,” Bloom said. “Spinal cord injury is an area where there’s a lot of interest in how the immune response impacts the injury acutely and how the injury impacts the immune response in the long term in the chronic phase.”

Bloom also worked with scientists from the University of Kentucky and Icahn School of Medicine at Mount Sinai.

“What we did in this study was identify all the genes that get turned on or off during that process of recovery,” Bloom said. “Neurobiology has a long history of using different species to understand specific scientific questions.”

The study reveals that some of the genes that repair an injured spinal cord in the lamprey, a jawless fish that shared a common ancestor with humans about 550 million years ago, are also active in the peripheral nervous system repair in mammals.

Bloom said lampreys can go from paralysis to full swimming behaviors in about 10 to 12 weeks with no medication or treatment, which spurred her study on how the lamprey’s synapses work and how its nerve cells communicate.

Bloom said infections are the leading cause of death for people with spinal cord injuries.

“Initially when people are injured, there’s an inflammatory response, but what can happen is response can get overheated and there can be adverse affects with the response itself,” Bloom said. “Nerve cells that are damaged could be in vulnerable state after the injury and the inflammation can exaggerate the loss of nerve cells.”

While the goal of the study is to figure out how to turn on or off the right genes to help nerve cells regenerate better, Bloom said this is a very long-term goal.


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