The primary focus of my lab is to examine the underlying molecular mechanisms that drive the development of Alzheimer’s disease (AD) and Parkinson’s disease (PD), the two most common forms of age-related neurodegeneration. My lab uses stem cells, including patient-derived induced pluripotent stem cells (iPSCs), to study the role of neural and immune cell populations in these disorders. We also generate and use transgenic mouse models of AD and PD to test potential therapies and examine the relationships between peripheral and central immunity and their influence on disease progression. Among our current studies, we are using iPSCs to generate human microglia and understand the effects of disease-associated genetic risk factors on microglial function and AD pathology. Working with immune-deficient AD mouse models, we have also recently uncovered an important role for the adaptive immune system in AD, finding that peripheral immune populations slow the development of beta-amyloid pathology by modulating microglial function. In collaboration with colleagues in the UCI Institute for Immunology, Dr. Blurton-Jones is now further examining the role of peripheral immune senescence in AD and determining precisely which adaptive immune cell populations are responsible for the observed effects on disease progression.

Stem cells, Parkinson's disease, Alzheimer's disease, neurogenesis, neurodegeneration