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Eva Feldman

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Primary Appointment:
Primary PIBS Dept.: Neuroscience
Other PIBS Depts.: Bioinformatics
PubMed Name: Feldman EL
Department Website
Lab Website

  I am interested in understanding the pathogenic mechanisms that trigger neurodegeneration in the central and peripheral nervous systems and identifying effective therapies. I direct a multifaceted research program encompassing basic science, clinical and translational research.

In the laboratory, we harness the advantages of cellular disease models, animal disease models, stem cell biology, and computer-based analyses in order to gain comprehensive insight into disease processes. Specific projects are detailed on our website ( and focus on understanding how conditions such as diabetes, Alzheimer’s disease (AD), and amyotrophic lateral sclerosis (ALS) damage nerve cells. Our diabetic neuropathy research program combines cell and animal models and human tissues with advanced molecular and bioinformatics analyses to characterize and understand the mechanisms underlying nerve damage associated with diabetes. Specifically, we are identifying genetic transcripts, proteins, and metabolites that are altered in both diabetic patients and rodent models with diabetic complications to identify common mechanisms and molecular responses in complication-prone tissues, as well as examining energetic pathways involved in the onset of complications in nerve, kidney, and eye through collaborative efforts to define the specific changes in cellular substrate metabolism that drive the development of diabetic complications. Our multifaceted neurodegenerative disease research program involves in vitro, in vivo, and clinical research to elucidate the mechanisms and develop novel therapies for ALS and AD. Briefly, we have developed cellular models of ALS expressing mutant forms of TDP-43, a protein linked ALS pathogenesis, to examine disease pathogenesis and screen potential therapies. We have also established the University of Michigan ALS Patient Repository (UMAPR) which contains viable biospecimens from ALS subjects and healthy controls paired with robust clinical data. These unique resources are being utilized to identify potential ALS risk factors associated with environmental exposures and to characterize how epigenetic modifications impact gene expression and contribute to the development of ALS. In addition, we are examining the therapeutic potential of newly developed stem cell lines in the treatment of ALS, and examining the efficacy of intracranial cellular transplantation in an animal model of AD as a demonstration of the translational potential of our ALS cellular therapy strategies to other neurological disorders

Overall, the knowledge gained from these projects will identify targets that are most amenable to conventional or novel therapies, identify biomarkers that offer diagnostic and prognostic advantages, and enable development of new comprehensive treatment strategies that can be translated to patients