Research in Hub 4 strives to go beyond the “beta amyloid hypothesis” of Alzheimer’s disease (AD) to address other factors contributing to AD and related forms of dementia. There are two major goals: 1) use interdisciplinary approaches to gain insight into disease mechanisms and develop treatments for dementia-related proteinopathies; 2) understand the relationship between altered metabolism and dementia symptom onset and disease severity. The research is driven by a multi-disciplinary team that includes experts in chemistry, pharmacology, pharmaceutical sciences, nutritional sciences, molecular biology and genetics, animal behaviors, clinical research, and patient care.
All meetings begin at 1:00 pm in room 5243 Life Sciences Institute
September 11, 2019
November 13, 2019
January 8, 2020
February 19, 2020
March 11, 2020 (canceled-meeting to be scheduled in April)
May 13, 2020
Geoffrey Murphy is an Associate Professor in the Department of Molecular and Integrative Physiology and an Associate Research Professor in the Molecular and Behavioral Neuroscience institute. The Murphy lab is interested in neurological disease states including Alzheimer’s disease and temporal lobe epilepsy. In addition the lab is investigating the neural substrates that underlie complex psychiatric diseases such as bipolar.
Bing Ye is the Burton L. Baker Collegiate Professor of the Life Sciences and an associate professor of cell and developmental Biology. His laboratory studies how neuronal development contributes to the assembly and function of nervous systems and how defects in this process lead to diseases. The Ye lab collaborates with chemists and pharmaceutical scientists to develop therapeutic strategies for brain disorders.
Hank Paulson’s laboratory seeks to understand the mechanisms underlying neurodegenerative proteinopathies including polyglutamine diseases, frontotemporal dementia and Alzheimer’s disease. We use approaches ranging from in vitro analysis of recombinant proteins to mouse models of disease. Two major areas of focus are the polyglutamine disorder Spinocerebellar Ataxia type III (SCA3) and the Ubiquilin family of proteins implicated in numerous forms of neurodegeneration. In translational studies, we have identified compounds and developed gene silencing strategies that decrease levels of the toxic jean product in SCA3. In addition to co-directing the PFD Initiative, I direct the NIH-funded Alzheimer’s Disease Center at the University of Michigan.
Magdalena Ivanova is a Research Assistant Professor in the Department of Neurology and Adjunct Assistant Professor in the Program of Biophysics. Her laboratory applies biophysical and biochemical based approaches to study protein misfolding and aggregation in association with neurodegenerative diseases. The ultimate goal is to exploit the acquired information for developing therapies that may slow, delay, inhibit, or reverse neurodegeneration.
Peter Tessier is the Albert M. Mattocks Professor of Pharmaceutical Sciences, Chemical Engineering and Biomedical Engineering. His lab aims to develop next generation technologies for designing, discovering, engineering, characterizing, formulating and delivering biologics ranging from small affinity peptides to large monoclonal antibodies for molecular imaging, diagnostic and therapeutic applications. The Tessier lab is particularly interested in generating conformational antibodies that are selective for different types of soluble and insoluble aggregates linked to Alzheimer’s, Parkinson’s and other neurodegenerative diseases.
Lisa Sharkey’s research interests focus on the consequences of protein mis-folding in neurodegenerative disease. She primarily studies Ubiquillin2, a quality control protein which when mutated causes a spectrum of human neurodegenerative disease including ALS and ALS/FTLD. In addition, she is investigating the effects of protein homeostasis on brain health and cognitive aging.