Dr. Hayley McLoughlin is an Assistant Professor in the University of Michigan Neurology Department, with a joint appointment in the Department of Human Genetics. She earned her Neuroscience doctoral degree in 2013 from the University of Iowa in Dr. Beverly Davidson's laboratory and completed a postdoctoral research fellowship under the guidance of Dr. Henry (Hank) Paulson at the University of Michigan. In her postdoc, she assessed the efficacy of antisense oligonucleotide therapy in mouse models of Spinocerebellar Ataxia type 3/Machado-Joseph disease (SCA3/MJD). In 2016, she was appointed to research faculty at the University of Michigan where her lab focuses on establishing pathogenic mechanisms and therapeutic interventions for neurodegenerative diseases with particular emphasis toward the polyglutamine disease, SCA3. SCA3 is a progressive, dominantly inherited neurodegenerative disease for which there currently is no treatment. Dr. McLoughlin has recently been appointed to the tenure-track at the University of Michigan, where she continues to lead SCA3 preclinical efforts toward antisense oligonucleotide (ASO) gene silencing and viral-mediated RNAi in collaboration with industry partners. In hopes of identifying additional routes for therapeutic intervention, discovery of novel disease biomarkers, and to provide broader insight into the polyglutamine diseases beyond SCA3, the McLoughlin lab also interrogates disease mechanisms using a variety of SCA3 cellular and animal disease models as well as human tissue and biofluid samples.
Areas of Interest
The McLoughlin lab uses a series of cell and mouse models coupled with analysis of human disease tissue to assess the following research focuses:
1. Nonneuronal contributions to neurodegeneration: Our work investigates a significant gap in our understanding of SCA3 and other polyglutamine diseases: nonneuronal contributions to disease pathogenesis, specifically cells of the oligodendrocyte (OL) lineage. Studying their role in disease will define whether OLs need to be a target of emerging therapies, shed light on the importance of communication between neurons and glia in polyQ disease pathogenesis, and may identify robust OL biomarkers of disease progression that will aid in clinical trial endpoints.
2. Therapeutic development for SCA3:
Because expression of the mutant ATXN3 protein is an early and necessary step in SCA3 disease pathogenesis, strategies to reduce expression of the disease gene or enhance clearance itself are high on the list of potential therapies. The lab is currently pursuing three preclinical research programs: a. ASO therapy; b. Viral-mediated RNAi therapy; c. Viral-mediated chaperone therapy. As a supplement to many of these programs, the lab is also assisting in the discovery and development of disease biomarkers.
- PhD, Neuroscience with honors, University of Iowa, 2013
- Post-doctoral Research Fellow, Internal Medicine, University of Iowa, 2014
- Postdoctoral Research Fellow, Neurology, University of MIchigan, 2016