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Effect of intranasal HB-EGF treatment on brain glucose metabolism and inflammation after TBI in the developing brain

Award Number: R21NS131048
ORGANIZATION: NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)
PERIOD OF PERFORMANCE START DATE: 06/01/2025
PERIOD OF PERFORMANCE END DATE: 05/31/2027

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Effect of intranasal HB-EGF treatment on brain glucose metabolism and inflammation after TBI in the developing brain - Pediatric traumatic brain injury (TBI) is the leading cause of significant life-long cognitive and sensorimotor disabilities. To date, acute care is limited to supportive measures, and there continues to be a lack of targeted therapeutics to improve neurologic outcome. Metabolic crisis from impaired oxidative glucose metabolism and inflammation are the hallmarks of TBI. The dysregulation and impaired mitochondrial function results in the depletion of energy in the form of ATP. Simultaneously, TBI is characterized by activation of microglia – the resident macrophages of the brain – to clear damaged tissue. The ongoing secondary injury due to mitochondrial dysfunction and decreased cell viability signal the microglia to remain in a persistently activated state, becoming dysregulated and further propagating the inflammatory cascade. Targeted therapy that improves oxidative glucose metabolism and limits inflammation is crucial. Recent data from our lab found that a neurotrophic growth factor, heparin-binding epidermal growth factor (HB-EGF) increases pathways responsible for oxidative phosphorylation and decreases inflammation. Our preliminary experiments suggest that intranasal HB-EGF quickly enters the brain and improves mitochondrial health. Therefore, we hypothesize that treatment with intranasal HB-EGF after moderate-severe pediatric TBI will improve brain oxidative glucose metabolism and mitochondrial function while decreasing inflammation. In the first aim, we will determine whether treatment with intranasal HB-EGF after TBI improves brain oxidative glucose metabolism and delineate the regional and temporal effects of intranasal HB-EGF after developmental TBI. In the second aim, we will determine whether treatment with intranasal HB-EGF in the acute period after TBI decreases inflammation. The impact of this project is that we will gain a greater understanding of the regulation of metabolism and inflammation from treatment with HB-EGF in normal and injured developing brain.


Issue Date FY	Funding FY	Legal Entity Name	Legal Entity Address	Legal Entity City	Legal Entity State	Legal Entity Zip Code	Legal Entity COUNTY	Legal Entity COUNTRY	Assistance Listing	Award Code	Budget Year	Action Date	Action Type	Action Amount

Issue Date FY: 2025 ( Subtotal = $453,970 )
2025	2025	HUGO W. MOSER RESEARCH INSTITUTE AT KENNEDY KRIEGER, INC.	707 N BROADWAY	BALTIMORE	MD	21205	BALTIMORE CITY	USA	Extramural Research Programs in the Neurosciences and Neurological Disorders	000	1	5/23/2025	NEW	$453,970
														Subtotal = $453,970

Grand Total All Awards = $453,970

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Effect of intranasal HB-EGF treatment on brain glucose metabolism and inflammation after TBI in the developing brain

Award Number: R21NS131048

ORGANIZATION: NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)

PERIOD OF PERFORMANCE START DATE: 06/01/2025

PERIOD OF PERFORMANCE END DATE: 05/31/2027

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