Irving E. Vega, PhD
Associate Professor, Translational Neuroscience
Ph.D., 2002, Rutgers Graduate School of New Brunswick
Grand Rapids Campus
Grand Rapids Research Center
Our research program focuses on the identification and characterization of neuronal proteome changes associated with tau-mediated neurodegeneration in specific brain regions or body fluids (e.g. blood, cerebrospinal fluid). Tauopathies are neurodegenerative diseases in which the main pathological hallmark is the aggregation of the protein tau in specific brain regions. Tau is a microtubule associated protein that regulates the dynamic instability of microtubules in the neuronal axon. Hyperphosphorylation (and other posttranslational modifications) releases tau from its association with microtubules and made it prone to aggregation. Tau oligomers and tangles are found in distinct brain regions in diseases such as Alzheimer's disease (AD), Progressive Supranuclear Palsy (PSP), Frontetemporal dementia and Parkinsonism linked to chromosome 17 (FTDP-17) and others. The central pathological role of Tau proteins is underscore by the identification of dominant mutations on the Tau gene (MAPT) in diseases such as PSP and FTDP-17. However, despite the fact that several decades of research have provided insights into the molecular characteristics of pathological tau species, the etiology and pathobiology of tauopathies remain poorly understood. We conceive that deciphering how cells in specific brain regions respond to pathological tau could lead to the identification of no only neurodegenerative molecular mechanisms, but also neuroprotective cellular stress responses. Accordingly, we use genomics and proteomics approaches to analyze postmortem brain tissue from human tauopathy cases and animal tauopathy models, as well as in vitro cellular models for controlled mechanistic studies in order to gain insights about adaptive proteome responses to pathological tau species.