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The role of ABI3 in Alzheimers disease

Award Number: RF1AG074543
ORGANIZATION: NATIONAL INSTITUTE ON AGING
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)
PERIOD OF PERFORMANCE START DATE: 09/15/2021
PERIOD OF PERFORMANCE END DATE: 08/31/2024

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The role of ABI3 in Alzheimers disease - Project Summary/Abstract In recent large-scale genome-wide analysis studies, a rare coding variant was identified in Abelson interactor family member 3 (ABI3) gene and this variant is associated with increased risk of late-onset Alzheimer’s disease (LOAD). ABI3 is highly conserved across multiple species, including humans and mice. Interestingly, it is highly expressed in microglia and relatively more abundant in the hippocampus, compared to the other brain regions. The overarching goal of this application is to understand the role of ABI3 in microglia function and the mechanisms by which ABI3 affects the pathogenesis of AD. We propose the following Specific Aims to test our hypotheses. In Aim 1, we will determine the effect of Abi3 deletion on Alzheimer’s disease pathology using two mouse models. By performing unbiased transcriptomic and proteomic analyses, we will identify the potential key regulators of Abi3-mediated effects. We will conduct further functional and biochemical experiments to dissect the mechanism based on these findings. In Aim 2, we will investigate the effect of the ABI3 rare coding variant on AD pathology using ABI3 knock-in mouse model. We will perform brain imaging and electrophysiology experiments to assess the functional effects of ABI3 risk variant. In addition, we will assess neuropathological phenotypes in the brains. To identify the potential pathways and key regulators, we will analyze transcriptome and proteome altered by ABI3 knockout and knock-in. In Aim 3, we will perform microglial cellular assays to determine the effects of ABI3 risk variant on microglia functions. Furthermore, we will use RNA interference approach to knock-down the genes of our interest to dissect the mechanism behind the ABI3 risk variant- mediated changes. The successful completion of this study will provide novel insights into the mechanisms of AD, in particular, microglial functions mediated by Abi3. Our long-term goal is to identify new druggable targets for the effective treatment of AD.


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 = -$64,415 )
2025	2021	TRUSTEES OF INDIANA UNIVERSITY	980 INDIANA AVE RM 2232	INDIANAPOLIS	IN	46202	MARION	USA	Aging Research	000	1	12/19/2024	NEW	-$64,415
														Subtotal = -$64,415

Issue Date FY: 2022 ( Subtotal = $0 )
2022	2021	TRUSTEES OF INDIANA UNIVERSITY	980 INDIANA AVE RM 2232	INDIANAPOLIS	IN	46202	MARION	USA	Aging Research	000	1	1/4/2022	NEW	$0
														Subtotal = $0

Issue Date FY: 2021 ( Subtotal = $2,284,811 )
2021	2021	TRUSTEES OF INDIANA UNIVERSITY	980 INDIANA AVE RM 2232	INDIANAPOLIS	IN	46202	MARION	USA	Aging Research	000	1	9/13/2021	NEW	$2,284,811
														Subtotal = $2,284,811

Grand Total All Awards = $2,220,396

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The role of ABI3 in Alzheimers disease

Award Number: RF1AG074543

ORGANIZATION: NATIONAL INSTITUTE ON AGING

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

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

PERIOD OF PERFORMANCE START DATE: 09/15/2021

PERIOD OF PERFORMANCE END DATE: 08/31/2024

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