What You Need to Know
Hackensack Meridian Neuroscience Institute at JFK University Medical Center announced that it has been awarded a major research grant from the National Institute of Neurological Disorders and Stroke, part of the U.S. National Institutes of Health, to study a novel approach on whether the blocking of formation of Neutrophil extracellular traps (NET) provides better outcomes after a Traumatic Brain Injury (TBI). The five-year award of $2,213,750 is part of the highly competitive NIH extramural grant application process that recognizes innovative scientific projects. NIH-funded research has led to scientific breakthroughs and new treatments that help people live longer, healthier lives.
The NIH grant 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, Research Scientist & Principal Investigator, Hackensack Meridian Neuroscience Institute at JFK University Medical Center, and Associate Professor of Neurology at the Hackensack Meridian School of Medicine.
The work hypothesizes that inhibition of peptidyl arginine deiminase type 4 (PAD4), an enzyme required for NET formation, using PAD4 antagonistic peptide (PAP), will attenuate the formation of NET, NET-induced thrombosis, and will promote neovascularization and functional recovery after TBI.
The Muneer lab at the Hackensack Meridian Neuroscience Institute seeks to demonstrate a unique therapeutic strategy for TBI focusing on the activation of leukocytes, especially neutrophils that cause the release of nuclear and granular contents to form an extensive web-like structure of DNA called neutrophil extracellular traps (NET). In TBI, the mechanism of injury-induced formation of NET and its mechanistic regulatory role in thrombosis have remained elusive. Moreover, it is unclear whether blocking NET formation provides better outcomes after TBI. Therefore, Dr. Muneer’s novel research efforts to suppress the formation of NET will provide critical information potentially supporting a valuable new therapeutic strategy to enhance functional recovery following TBI.