Our Research
Alzheimer’s disease (AD) is the leading cause of dementia with an estimated prevalence of more than 6 million people in the United States alone. AD research has become increasingly important as cases continue to rise each year. In the Huang lab at Brown University, we use human stem cell-based models to investigate the biological drivers of AD in the pursuit of more efficacious therapeutic development.
Our current research endeavors include:
Human stem cell model development
To accurately model AD biology in vitro we utilize methods to differentiate human stem cells into the various lineages of central nervous system cell types. We currently use, and are optimizing, methods to generate all 4 major brain cell types: neurons, astrocytes, oligodendrocytes, and microglia. This approach allows us to take a reductionist approach to investigate cell-specific biological phenomena. It also allows us to study the complex interplay between each cell type.
Autophagy & Endosomal Dysfunction in AD
Autophagy is the main bulk protein degradation pathway in neurons and it is known to be dysfunctional in AD: a disease characterized by the buildup of toxic proteins in the brain. One main area of research in the Huang lab is investigating the relationship between a major AD genetic risk factor and autophagic as well as endosomal dysfunction. Our goal is to better define the genetic risk factor, and reveal how this alteration can disrupt these critical homeostatic pathways.
Neuroinflammation in AD
AD-associated neuroinflammation has gained traction as a potential causative factor in disease pathogenesis. One of our research goals is to expand on current research surrounding a well-known AD biomarker, and characterize its potentially causative role in this disease. Since the neuroinflammatory process involves the activity of multiple cell types we can leverage our stem cell technologies to accurately model this phenomenon.
Myelination deficiency in Angelman Syndrome
In addition to our projects focused on neurodegeneration, we also have a research effort to investigate the pathogenesis of a neurodevelopmental disease: Angelman Syndrome. This disease has a known genetic etiology which causes developmental delay and various neurological sequelae in children. We are researching how disease genetics can impact oligodendrocyte function, the major myelinating cell type in the central nervous system.
iNeuron
iAstrocyte
iMicroglia iOligodendrocyte