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Extracellular Vesicles of iPSC-derived Brain Organoids as Therapeutic Targets for Alzheimer’s Disease

Award Number: R01AG090809
ORGANIZATION: NATIONAL INSTITUTE ON AGING
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)
PERIOD OF PERFORMANCE START DATE: 09/01/2026
PERIOD OF PERFORMANCE END DATE: 08/31/2031

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Extracellular Vesicles of iPSC-derived Brain Organoids as Therapeutic Targets for Alzheimer’s Disease - PROJECT SUMMARY/ABSTRACT The accumulation, aggregation, and deposition of amyloid-β (Aβ) and tau in the brain accompanied with neurodegeneration are central events in the pathogenesis of Alzheimer’s disease (AD). AD is a progressive neurodegenerative disease, which is the leading cause of dementia in the elderly. Whereas the spatial progression pattern of Aβ and tau pathologies differs in the brains, Aβ and tau lead to neurodegeneration in a synergic manner during the progression of AD. Therefore, to determine the molecular mechanisms underlying the complex AD pathogenesis and identify potential therapeutic targets, the greater understanding of cross-talk between Aβ and tau in the disease development and progression might be critical. In particular, extracellular vesicles (EVs) play an important role in maintaining tissue homeostasis, by modulating immune system, senescence, proliferation and differentiation in various biological processes. We hypothesize that tau, Aβ, and EVs interactively trigger the pathogenic cascades for neurodegeneration in AD. Furthermore, susceptible loci for late-onset AD including APOE predominantly express in microglia, which causatively or consequently participate in the molecular mechanisms in the disease. Thus, in this proposal, we will comprehensively address tau- and Aβ-related phenotypes using innovative induced pluripotent stem cell (iPSC)-derived 3-D models composed of dorsal/ventral brain organoids and microglia as well as mouse models, and evaluate the contributions and the therapeutic benefits of EVs to the pathogenic phenotypes through proteomics and miRNA profiling. The combination of human iPSC organoid technology, EV engineering, and animal models with targeted and non-targeted approaches should allow us to both test hypotheses and generate potential therapeutics in our collective efforts to address the synergic roles of tau and Aβ in neurodegeneration, and involvements of microglia and EVs in the pathogenic pathways. In Aim 1, we will examine tau- and Aβ-related phenotypes in iPSC-derived brain organoids. We will define how genetic backgrounds in microglia impact tau- and Aβ-related phenotypes in the 3-D organoid AD models. In Aim 2, we will examine the contributions of EVs to the pathogenic phenotypes in the 3-D organoid models. In Aim 3, we will engineer EVs from the iPSC-derived organoids and reveal the therapeutic effects of EVs in mouse AD models. Collectively, these studies enable us refining how Aβ and tau lead to neurodegeneration, which is highly significant in developing novel therapeutic strategies for 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: 2026 ( Subtotal = $664,279 )
2026	2026	FLORIDA STATE UNIVERSITY	874 TRADITIONS WAY	TALLAHASSEE	FL	32306	LEON	USA	Aging Research	000	1	9/1/2026	NEW	$664,279
														Subtotal = $664,279

Grand Total All Awards = $664,279

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Extracellular Vesicles of iPSC-derived Brain Organoids as Therapeutic Targets for Alzheimer’s Disease

Award Number: R01AG090809

ORGANIZATION: NATIONAL INSTITUTE ON AGING

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

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

PERIOD OF PERFORMANCE START DATE: 09/01/2026

PERIOD OF PERFORMANCE END DATE: 08/31/2031

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