NIH awards $2.2M grant to advance research for novel therapy to improve TBI recovery

Key takeaways:

• The National Institute of Neurological Disorders and Stroke awarded $2.213 million over 5 years.
• Research will center on a novel peptide which activates leukocytes to promote functional TBI recovery.

The National Institute of Neurological Disorders and Stroke has awarded a grant to researchers at Hackensack Meridian Neuroscience Institute to study a novel approach to improving outcomes after TBI.

According to a release issued by Hackensack Meridian Neuroscience Institute at JFK University Medical Center, the grant amounts to $2,213,750 over 5 years. It will fund a project entitled “Neutrophil extracellular traps and associated pathogenesis in TBI: A novel peptide therapeutic strategy” proposed by Mohammed Abdul Muneer, MSc, PhD, associate professor of neurology and principal investigator at the health organization.

"This novel project will be a milestone in contributing to the advancement of designing therapeutic interventions in clinical settings against [traumatic brain injury],” Muneer told Healio in an email. “Once safety, efficacy, and understanding of this particular peptide therapy are optimized, there is a promise that this peptide therapy will move quickly into clinical trials.”

Muneer’s lab intends to demonstrate a novel therapeutic strategy for TBI centered on activation of leukocytes, particularly neutrophils responsible for release of nuclear and granular contents to form an extensive weblike structure of DNA called neutrophil extracellular traps (NET).

Per the release, the mechanism of injury-induced formation of NET and its mechanistic regulatory role in thrombosis that accompanies TBI are still unclear. Also unclear is whether blocking NET formation provides better outcomes after TBI, with Muneer’s team seeking to examine how NET suppression may provide critical information that is likely to support a new therapeutic strategy.

Muneer’s research further hypothesizes that inhibition of peptidyl arginine deiminase type 4 (PAD4), an enzyme required for NET formation, using PAD4 antagonistic peptide, will attenuate the formation of NET and NET-induced thrombosis, and promote neovascularization and functional recovery after TBI.