# Utilization of proteomics and lipidomics to identify modifiers of LBD

> **NIH NIH U54** · MAYO CLINIC  JACKSONVILLE · 2020 · $674,800

## Abstract

Summary
The long-term goal of this project is to define dysfunctional molecular networks underlying the pathogenesis of
Lewy body Dementia (LBD) disease, and the synergistic interaction of amyloid-beta and alpha-synuclein,
primarily by omics-based systems biology approaches, focusing on proteomics and lipidomics using cutting-
edge mass spectrometry (MS) in Project 2. LBD is the second most common cause of progressive dementia and
shares characteristics with Alzheimer's disease (AD) and Parkinson's disease (PD). It is characterized by the
manifestation of Lewy body (alpha-synuclein) pathology and amyloid plaques (amyloid-beta) in the brain.
Clinically, LBD is associated with dementia, psychosis, and features of PD. Identifying clinically relevant
molecules (DNAs, RNAs, proteins, or metabolites) is essential to predict, diagnose, treat, and prevent LBD.
Complementary to the genome and transcriptome profiling in Project 1, Project 2 seeks to fully characterize the
whole proteome, aggregated proteome, posttranslational modifications, and lipidome directly from well-
characterized LBD and control brain specimens with different pathologies (provided by Core B). To achieve this
goal, we have assembled a strong multidisciplinary team with established and renowned investigators in
proteomics (Peng) and lipidomics (Han), both also having extensive expertise in studying neurodegeneration
including analyzing human brain tissues. We will focus on three specific aims: (i) to identify aberrant protein
networks in LBD with different pathologies by profiling the whole proteome; (ii) to integrate multiple-tier
proteomics approaches to define LBD by profiling aggregated proteome, phosphoproteome and ubiquitinome;
and (iii) to determine LBD pathways by lipidomics profiling. The acquired omics data will provide a rich resource
for hypothesis-driven research, and will be integrated for generating a precise molecular signature shared in LBD
cases, categorizing possible LBD subtypes, revealing key molecular dysfunction, especially linking the
interaction of amyloid-beta and alpha-synuclein.

## Key facts

- **NIH application ID:** 10022183
- **Project number:** 5U54NS110435-02
- **Recipient organization:** MAYO CLINIC  JACKSONVILLE
- **Principal Investigator:** JUNMIN PENG
- **Activity code:** U54 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $674,800
- **Award type:** 5
- **Project period:** 2019-09-20 → 2024-06-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10022183

## Citation

> US National Institutes of Health, RePORTER application 10022183, Utilization of proteomics and lipidomics to identify modifiers of LBD (5U54NS110435-02). Retrieved via AI Analytics 2026-05-22 from https://api.ai-analytics.org/grant/nih/10022183. Licensed CC0.

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