Characterizing myeloid nuclear differentiation antigen (MNDA) in alzheimer's disease

Active Project Grant Awarded Last action

Award ID
F31AG099446
Recipient
Awarding agency
Obligated
$79,064

Award facts

Assistance listing
93.866 Aging Research
Completion date 0% complete
Originally
Place of performance
Galveston, TX 77555, USA

Award details come from USAspending.gov.

Description

As the agency reported it.

Abstract
Alzheimer's disease (ad) is a chronic, progressive neurodegenerative disorder of the central nervous system (CNS) that leads to cognitive impairment and remains a significant global health challenge among the aging population. Despite advancements in therapeutics, the cellular mechanisms underlying ad-particularly the neuronal phenotypes of the CNS and their complex intracellular functions-are not fully understood. Our lab specializes in characterizing trna-derived RNA fragments (TRFS), a recently discovered class of small non- coding rnas (SNCRNAS), and their roles in neurodegenerative diseases. We previously reported that TRFS represent the most abundant sncrna population in the hippocampus of ad patients. These ad-affected TRFS originate from a limited subset of mature trnas, with some showing functional correlations to disease severity. Among these, a TRF derived from the 5'-end of the trna encoding GLYCCC (TRF5-GLYCCC) has emerged as a key molecule of interest. Of surveyed ad patients by our lab, human serum samples provided a differentially expressed gene candidate that possibly contributes to dysregulated neuron function in ad. Preliminary data show that ad patients exhibit significantly elevated myeloid nuclear differentiation antigen (MNDA) levels in their serum, hippocampal tissues, and ipsc-derived neurons. Furthermore, our computational target prediction algorithms and experimental data suggest that MNDA is a potential target of TRF5-GLYCCC. The long-term goal of this project is to investigate the biological and health consequences of ad-affected TRFS to deepen our understanding of disease mechanisms. The objective of this grant is to determine how dysregulated MNDA impacts neuronal function and how this gene is regulated by ad-specific TRFS. We hypothesize that MNDA is a disease-associated gene in ad and that TRF5-GLYCCC contributes to its expression and regulation. In aim 1, the effects of MNDA on neuronal cell phenotypes in ad will be investigated. In aim 2, the regulatory interaction between TRF5-GLYCCC and MNDA will be characterized. Through this F31 fellowship, the conclusion of MNDA's function and regulation by TRFS would provide novel mechanistic insights into ad progression, particularly in diverse patient populations with sporadic forms of the disease. Additionally, I will acquire advanced skills in cell culture and molecular biology, including ipsc culture, cell differentiation/maturation, crispr/CAS9 gene editing, and various assays to evaluate neuronal phenotypes specific to ad. These methodologies will be standardized into protocols, contributing to both our lab and the broader fields of ad research and sncrna biology. These experiences will prepare me for my long-term career goal of becoming an independent molecular and neuroinflammatory research scientist.

Transactions

Action Obligated Date
Amendment $39,532
Amendment $39,532
Original award $0

Quick answers

Who received award F31AG099446?

F31AG099446 was awarded to University Of Texas Medical Branch At Galveston by National Institute on Aging (National Institutes of Health) on December 15, 2026.

How much is award F31AG099446 worth?

$79,064 has been obligated on F31AG099446.

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