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Defining the role of dysregulated circular RNA hsa_circ_0000119 in amyotrophic lateral sclerosis pathogenesis

Award Number: F30AG099720
ORGANIZATION: NATIONAL INSTITUTE ON AGING
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS
PERIOD OF PERFORMANCE START DATE: 03/10/2027
PERIOD OF PERFORMANCE END DATE: 03/09/2028

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Defining the role of dysregulated circular RNA hsa_circ_0000119 in amyotrophic lateral sclerosis pathogenesis - PROJECT SUMMARY This NIH F30 application describes the plan for mentored research and career development for the PI, Katherine “Kate” Ann Smith. The scientific premise of this proposal focuses on the role of a newly identified circular RNA (circRNA), hsa_circ_0000119 (circ119), in the pathogenesis of amyotrophic lateral sclerosis (ALS). ALS is an age-associated, progressive, and fatal neurodegenerative disease which affects upper and lower motor neurons. This degeneration leads to muscle atrophy and, ultimately, death within 3-5 years of diagnosis of the disease. The disease is typically diagnosed in people ages 40-70 years old. Because of the sporadic and heterogenous nature of ALS, researchers have faced difficulties studying the disease and devising effective therapies. A recent publication from the King Lab established a link between ALS and a relatively unexplored class of RNAs known as circRNAs. Several circRNAs were shown to be dysregulated in ALS patients and the SOD1G93A ALS mouse. Of the identified circRNAs in human tissue, circ119 was highly upregulated and first appeared at symptom onset in the ALS mouse and persisted throughout disease course. This proposal seeks to identify the role of circ119 in ALS pathophysiology by first characterizing the ribonucleoprotein complex (proteins and RNAs) associated with the circRNA (Aim 1) and its impact on motor neuron physiology (through circRNA silencing or overexpression), focusing on key disease-driving cellular processes including protein mislocalization/aggregation, splicing, and mitochondrial function (Aim 2). These findings will advance our understanding of ALS pathophysiology, as well as the biology of circRNAs in general and the roles they may play in neurodegenerative diseases and other related diseases of aging such as frontal temporal lobe dementia. The proposed training plan is sponsored by Kate Smith’s mentor, Peter King, MD. Included in the training plan are experiences which will help Kate Smith develop in three major areas: 1) rigorous training in key aspects of molecular biology and cellular communication, which includes support from experts in neurodegeneration, critical evaluation of data, and training in the responsible conduct of research; 2) rigorous training in bioinformatics and computational biology modeling, biochemical assays, and experiments using patient-derived induced pluripotent stem cell-derived motor neurons and organoids, and 3) career and professional development, including grant and manuscript writing, scientific communications, and the translation of research findings to clinical applications. This proposal will drive the development of skills required for rigorous scientific research for Kate future career as a physician-scientist in the field of age-related diseases of neurodegeneration.


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 = $43,996 )
2026	2026	UNIVERSITY OF ALABAMA AT BIRMINGHAM	701 S 20TH STREET	BIRMINGHAM	AL	35294	JEFFERSON	USA	Aging Research	000	1	9/10/2026	NEW	$43,996
														Subtotal = $43,996

Grand Total All Awards = $43,996

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Defining the role of dysregulated circular RNA hsa_circ_0000119 in amyotrophic lateral sclerosis pathogenesis

Award Number: F30AG099720

ORGANIZATION: NATIONAL INSTITUTE ON AGING

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS

PERIOD OF PERFORMANCE START DATE: 03/10/2027

PERIOD OF PERFORMANCE END DATE: 03/09/2028

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