Vega Lab
Lab Personnel
- Irving E. Vega, PhD, Principal Investigator, Director Integrated Mass Spectrometry Unit
- Jared Lamp, PhD, Manager Integrated Mass Spectrometry Unit
- Andrew Umstead, PSM, Lab Manager, Technician Integrated Mass Spectrometry Unit
- Ana Ramos, MSW, Community Engagement Coordinator
Current Funding
PF-CG-1503481
Parkinson’s Foundation
Supportive Alliance for Brain Education and Research (SABER): Parkinson's disease among Spanish Speaking Communities
Name of PD/PI: Vega
R25NS090989
ENDURE Bridge to the PhD in Neuroscience
Name of PD/PI: Vega
R01AG070951
Brain Health and Ethnic Disparities in ADRD Risk: The Case of Arab Americans
Name of PD/PI: Antonucci/Zahodne/Ajrouch
Role: PI Subaward
R01AG087121-01A1
ADRD risk and resilience among Black Americans a 20-year longitudinal study
Name of PD/PI: Mezuk
Role: PI Subaward
5P30AG072931
Michigan Alzheimer’s Disease Research Core
Name of PD/PI: Paulson
Role: Co-I, Co-Lead Research Education Component
P30AG053760-03S01
Michigan Alzheimer’s Disease Research Core-Supplement
Name of PD/PI: Paulson
Role: Lead
P30AG059300
Michigan Center for Contextual Factors in Alzheimer’s Disease (MCCFAD)
Name of PD/PI: Ajrouch/Antonucci/Zahodne
Role: PI Subaward, Lead – Community Liaison and Research Core
Publications
https://www.ncbi.nlm.nih.gov/myncbi/irving.vega.2/bibliography/public/
Overview
Pathological Tau Aggregation Project
Tau aggregation is a pathological hallmark in Alzheimer’s disease (AD) and other neurodegenerative diseases, known collectively as tauopathies. The lack of effective treatments that prevent or halt tau aggregation contributes to an increasing healthcare and economic burden for patients and caregivers. The evidence so far indicates that, longitudinally, tau undergoes conformation changes that lead to the formation of oligomers and, subsequently, filaments that tend to aggregate further into an ultrastructure known as neurofibrillary tangles (NFTs). An important conundrum related to the pathophysiology associated with tau-mediated neurodegeneration is deciphering the molecular processes that influence the transition of physiological tau monomers to pathological tau toxic species.
Our lab identified EFhd2 as a tau-associated protein that copurified and colocalized with tau filamentous structures found in AD cases. We have primarily focused on studying how the interaction between EFhd2 and tau induces the formation of tau aggregates. Our lab uses a comprehensive approach to study the effect that EFhd2 exert on tau protein dynamics ranging from molecular biology, protein biochemistry, mouse models and human tissue samples.
The overall goal of this project is to assess the role of EFhd2 in tau-mediated neurodegeneration and facilitate the establishment of models that can be used to test potential therapeutics against specific pathological tau toxic species.
Brain Microbial Proteome in Alzheimer’s
Alzheimer’s disease (AD) continues to be a major health issue in the US. Thus, it is imperative to better understand molecular processes that influence brain function and health. Several studies suggest that dysbiosis may modulate the inflammation associated with AD pathobiology. However, the relationship between dysbiosis and disease state is still poorly understood. Currently, there is no evidence of the establishment of a brain microbiota that directly influence the central nervous system, explaining how dysbiosis could lead to neurodegeneration.
Our lab focusses on uncovering the presence of specific bacterial species in normal aging and AD brain, and to enhance the understanding between dysbiosis and neurodegeneration. To achieve these goals, we developed an unbiased proteomics approach and stringent datamining pipeline to identify bacterial proteins in normal aging and AD brain tissue from two different brain banks.
The main goal of this project is to demonstrate that changes in brain microbiota influence health and disease. This information will contribute to understanding the mechanisms underlying the role of dysbiosis in neurodegeneration and will set the basis for a study of restoration and prevention.
Proteome Underlying Selective Vulnerability in Alzheimer’s Project
Studies directed to uncover the molecular environment that foster the generation and accumulation of pathological tau proteins are imperative to cease the epidemic of Alzheimer’s disease (AD) and related dementias. Selective brain vulnerability is a pathological aspect that needs to be better understood. Although aggregation of Ab peptides seems to precede tau pathology, it is the pathological aggregation of aberrantly phosphorylated tau proteins at specific brain regions what directly correlate with clinical presentation.
Our lab focuses on the identification of global proteome changes and differential tau interactome in specific brain regions to uncover factors associated with selective brain vulnerability. We use an integrated proteomics-computational approach to 1) identify tau-associated proteins and differential protein abundance within specific brain regions and 2) systematically characterize their convergence on to a genome-scale protein interaction network that explains selective vulnerability in AD.
The identification of brain region specific tau-induced proteome changes will serve as foundation to better understand molecular mechanisms associated with disease progression and selective vulnerability, which could lead to the development of therapeutic and/or prevention strategies.
Peripheral Biomarkers in Alzheimer’s Disease and Related Dementias
Alzheimer’s disease (AD) affects millions of people in the United States, and the number of cases is expected to rise dramatically in the coming decades. Developing reliable and minimally invasive diagnostic tools is essential for early detection and for evaluating potential disease-modifying treatments.
Our research focuses on peripheral biomarkers for AD and related dementias, including blood-based and nasal swab approaches. We aim to establish robust methods to measure key biomarkers such as tau and amyloid-beta peptides, while also discovering novel markers that improve diagnostic accuracy. Using quantitative and targeted proteomics, we seek to advance biomarker science beyond traditional cerebrospinal fluid and imaging techniques.
A critical component of this work is understanding how contextual and social factors influence biomarker variability. These factors can affect biomarker abundance and interpretation, which has important implications for accurate diagnosis and equitable treatment. By integrating molecular analysis with population-based research, this project addresses both biological and social determinants of health to ensure diagnostic strategies are effective across diverse communities.
The successful completion of this work will enhance the use of peripheral biomarkers as practical and inclusive tools for Alzheimer’s disease and related dementias.
Latino Community Network Approach to Address Risk Factors for Alzheimer’s Disease and Related Dementias
Latinos face a higher prevalence of Alzheimer’s disease (AD) compared to other populations, partly due to differential exposure to known risk factors such as cardiovascular disease, diabetes, and limited access to preventive healthcare. Traditional research approaches often prioritize recruitment and data collection without creating meaningful pathways for knowledge exchange or actionable change within the community. This gap between scientific discovery and practical application limits the impact of research on improving health outcomes.
Our goal is to shift from a research-centered model to a community- and person-centered approach that builds trust and fosters collaboration. Through the Latino Community Network, we engage local leaders, healthcare providers, and research institutions to identify contextual factors that contribute to increased risk and to co-develop strategies that promote brain health across the lifespan. This approach emphasizes bidirectional communication, ensuring that findings are shared with the community in ways that inform prevention, care practices, and resource access.
By creating a bridge between knowledge generation and real-world practice, this initiative seeks to reduce health gaps and empower communities to take an active role in shaping solutions for Alzheimer’s disease and related dementias.