The Gordon Neuroimaging Lab focuses on understanding the complexities of the aging brain. This includes studies of both healthy aging as well as neurodegenerative diseases such as Alzheimer disease. We integrate cognitive testing alongside advanced neuroimaging techniques, including MRI (volumetric, DTI, and fMRI) and PET imaging (amyloid, tau, and FDG). Our research crosses multiple domains and is at the intersection of cognitive neuroscience, psychology, neurology and radiology.
For the last 25 years, the Holtzman lab has been trying to better understand mechanisms underlying neurodegeneration, particularly as they are relevant to Alzheimer’s disease (AD). The lab has published extensively on the neurobiology of apoE and its receptors, how apoE, Aβ binding molecules, and other factors such as neuronal activity, glucose, insulin, and sleep influence Aβ metabolism.
A guiding principle of the Hope Center is that cell and molecular biological processes that underlie neurodegeneration are similar across disorders, such that research findings can be leveraged to provide insight beyond just one disease. Through the organization of research groups, the Hope Center aims to promote the sharing of unpublished data, foster collaboration, and speed the process of translation.
The goal of the Karch lab is to understand the molecular and cellular mechanisms underlying tauopathies. Defining the molecular mechanisms underlying tauopathies requires unraveling the complexities of the MAPT gene that encodes the tau protein, tau protein dysfunction within the cell, and the cell-cell interactions that produce pathology in the human brain. We use traditional immortalize and primary culture models in combination with human induced pluripotent stem cell-derived neuron and astrocytes. Defining the molecular and cellular mechanisms underlying tauopathies will improve our understanding of how tau genetics influences tau biology and will inform novel avenues for therapeutic intervention.
The Kipnis Lab investigates how the nervous and immune systems talk to each other in health and disease. Their goal is to elucidate the cellular and molecular mechanisms underlying nervous and immune system interactions in neurodegenerative, neurodevelopmental and mental disorders as well as in physiology (healthy aging).
The Lucey Lab investigates the relationship between sleep, aging and Alzheimer disease. Recent evidence suggests a role for sleep in Alzheimer disease pathogenesis and/or as a marker for the onset and/or progression of Alzheimer disease that could be followed as an outcome measure in treatment trials. The major goal of our research is use sleep to prevent or delay Alzheimer disease.
The Musiek Lab is focused on identifying and understanding molecular mechanisms of neurodegeneration in the mammalian brain. The Lab studies the circadian clock system and how it regulates glia function, neuroinflammation, protein aggregation, and neurodegeneration.
Areas of current interest include:
Circadian clocks in Alzheimer’s Disease pathogenesis
Regulation of glial function and neuroinflammation by the circadian clock
Interplay between aging, the circadian clock, and neurodegeneration
The role of glial cells in neurodegenerative diseases
Novel therapeutic targets for Alzheimer’s Disease
The clinical translational research of the Participation, Environment and Performance Laboratory (PEPL) focuses on the unique contribution that the environment can make toward improving the performance, participation and quality of life for persons living with functional limitations. Dr. Susy Stark and her team study how the environment accounts for the differences between what individuals are capable of doing and their actual participation. An exploration of the physical environment as influencing behavior is the basis of research questions studied by the lab. Most studies focus on the challenges faced by older adults in underserved communities in urban St. Louis.
The Snider Lab is interested in exploring how neurons die in neurodegenerative disorders and stroke, with a specific focus on how abnormally folded proteins, such as amyloid b-peptide and polyglutamine-containing proteins, cause neuronal death. These proteins are involved in the pathogenesis of Alzheimer disease and several dominantly inherited neurologic diseases, such as Huntington’s disease, dentatopallidoluysian atrophy and several spinocerebellar ataxias.