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Elucidating the role of ARID5A in central nervous system inflammation

Award Number: F31NS149734
ORGANIZATION: NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS
PERIOD OF PERFORMANCE START DATE: 12/01/2026
PERIOD OF PERFORMANCE END DATE: 11/30/2027

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Elucidating the role of ARID5A in central nervous system inflammation - Project Summary/Abstract Microglia are the resident immune cells of the central nervous system (CNS), playing essential roles in both tissue maintenance and injury response. In diseases like multiple sclerosis (MS), persistent microglial activation drives neuroinflammation, axonal injury, and neurodegeneration. Yet, the molecular mechanisms that maintain chronic microglial activation remain poorly defined, and no approved therapies directly target this compartment of disease. Although transcriptomic profiling has traditionally guided our understanding of inflammation, these approaches provide limited resolution over the rapid and reversible gene expression changes required for immune homeostasis. Post-transcriptional mechanisms, particularly those mediated by RNA-binding proteins (RBPs), enable more nuanced control of RNA fate. RBPs are emerging therapeutic targets in neurological disease in neurons, however, their function in microglial inflammation is largely unexplored. This proposal focuses on ARID5A, an RBP I have found to be upregulated in lesion-associated microglia in MS and experimental autoimmune encephalomyelitis (EAE), a model for MS. Preliminary studies show that ARID5A is required for sustained expression of interferon-stimulated genes in microglia, suggesting a central role in maintaining chronic CNS inflammation. This project will test the hypothesis that ARID5A enables microglia to sustain inflammatory gene expression by regulating RNA at multiple post-transcriptional checkpoints. I will define the cell autonomous role of ARID5A in microglial activation during CNS autoimmunity (Aim 1), and how ARID5A controls protein output in inflammatory microglia using ribosome profiling (Ribo-seq) and RNA-seq in both primary mouse and human iPSC-derived microglia (Aim 2). By uniting transcriptomic, translational, and regulatory profiling across complementary in vivo mouse and in vitro human systems, this work will define how dysregulated post-transcriptional control disrupts immune balance in microglia and contributes to chronic CNS inflammation. The complementary expertise of the Yeo lab in RNA biology and the Mendiola lab in neuroinflammation provides an ideal environment to execute this research plan and prepare me for a career as a physician-scientist in neuroimmunology and functional genomics.


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 = $43,565 )
2026	2026	UNIVERSITY OF CALIFORNIA, SAN DIEGO	9500 GILMAN DR	LA JOLLA	CA	92093	SAN DIEGO	USA	Extramural Research Programs in the Neurosciences and Neurological Disorders	000	1	5/12/2026	NEW	$43,565
														Subtotal = $43,565

Grand Total All Awards = $43,565

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Elucidating the role of ARID5A in central nervous system inflammation

Award Number: F31NS149734

ORGANIZATION: NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS

PERIOD OF PERFORMANCE START DATE: 12/01/2026

PERIOD OF PERFORMANCE END DATE: 11/30/2027

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