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The Role of Mouse Zinc Transporter ZIP12 in Brain Development

Award Number: R15HD112892
ORGANIZATION: NATIONAL INSTITUTE OF CHILD HEALTH AND HUMAN DEVELOPMENT
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)
PERIOD OF PERFORMANCE START DATE: 04/24/2024
PERIOD OF PERFORMANCE END DATE: 03/31/2027

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The Role of Mouse Zinc Transporter ZIP12 in Brain Development - Large gaps in knowledge about the causative mechanisms of neurodevelopmental disorders are significant hurdles for prevention and possibly treatment. Thus, there is an unmet need to identify genetic and environmental factors that place young individuals at risk for neurodevelopmental disorders. Importantly, it is recognized that the genes that control nutrient metabolism can impact neurodevelopment through interactions with both genetics and environment. The long-term goal of this laboratory is to identify nutrient metabolism genes necessary for brain development and propose nutritional intervention strategies to prevent or ameliorate cognitive deficits. Previous research from this laboratory has shown that ZIP12 is a zinc transporter that is necessary for mouse neuronal development in vitro and Xenopus tropicalis frog embryogenesis and neural tube closure in vivo. However, it is unknown whether ZIP12 promotes brain function and neuronal development in mammals in vivo. The overall objective for this proposal is to establish that ZIP12 is a nutrient metabolism protein that is necessary for mouse neuronal development and cognitive function in vivo, thereby making it clear that ZIP12 (and the encoding gene, SLC39A12) is a candidate for inherited neurodevelopmental disorders. ZIP12 knockout (KO) mice lacking a functional ZIP12 protein will be used to achieve this objective. The central hypothesis is that ZIP12 KO mice have impaired brain zinc uptake, which manifests early in life as a reduction in neuronal development and leads to reduced cognitive performance lasting through early adulthood (and likely throughout life). This proposal will test this hypothesis through studies designed to ask 3 specific questions. First, how does the loss of ZIP12 in mice affect brain zinc metabolism (and other minerals)? Second, how does the loss of ZIP12 affect learning and memory? Third, how does the loss of ZIP12 affect neurobiological development during the postnatal and early adulthood periods? Completion of these studies will establish in a mammalian model that ZIP12 is a zinc uptake mechanism necessary for proper brain zinc distribution to ensure optimal brain and cognitive function. This is significant because genes that are necessary for brain function are candidate genes for inherited neurodevelopmental disorders. The knowledge gained from these studies can lead to nutritional strategies for promoting optimal brain development and function. Furthermore, these studies will reveal mechanisms of genetic susceptibilities to neurodevelopmental disorders that are sensitive to nutritional deficiencies and may be prevented through nutritional or pharmacological interventions.


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: 2024 ( Subtotal = $445,552 )
2024	2024	OKLAHOMA STATE UNIVERSITY	401 WHITEHURST HALL	STILLWATER	OK	74078	PAYNE	USA	Child Health and Human Development Extramural Research	000	1	4/24/2024	NEW	$445,552
														Subtotal = $445,552

Grand Total All Awards = $445,552

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The Role of Mouse Zinc Transporter ZIP12 in Brain Development

Award Number: R15HD112892

ORGANIZATION: NATIONAL INSTITUTE OF CHILD HEALTH AND HUMAN DEVELOPMENT

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

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

PERIOD OF PERFORMANCE START DATE: 04/24/2024

PERIOD OF PERFORMANCE END DATE: 03/31/2027

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