Aaron Burberry earned his doctoral degree from the University of Michigan working with Gabriel Nunez to understand host-microbial interactions in Crohn’s disease and hematopoietic stem cell response to infection. For post-doctoral studies, Aaron trained with Kevin Eggan at Harvard University where became interested in studying how a common inherited mutation causes neural degeneration in Amyotrophic lateral sclerosis (ALS) and Frontotemporal dementia (FTD). He and his colleagues discovered that this gene acts in the immune system including macrophages and T cells to restrict neural inflammation and autoimmunity in response to gut bacteria. Aaron received a K99/R00 Pathway to Independence award from the National Institute of Aging and joined the faculty at ÐÇ¿Õ´«Ã½ in 2021 as Assistant Professor in the Department of Pathology where he continues to explore genetic and environmental contributions to neural inflammation. To accomplish this, the Burberry group applies cutting-edge techniques such as single cell RNA sequencing, mass cytometry, and bacterial metatranscriptomics along with our innovative germ-free C9orf72 loss of function mice and human induced pluripotent stem cell derived models of microglia and motor neurons.
Neurodegenerative diseases impart a devastating toll on patients and their caregivers, while costing hundreds of billions in lost wages and healthcare annually. Rare genetic mutations and common genetic polymorphisms interact in surprising ways with the environment to shape each person’s relative risk of developing disease. Our research leverages patient biomaterial, human pluripotent stem cells and animal models to discover disease relevant pathways to ultimately enable innovative therapeutic strategies.
Teaching Information
Teaching Interests
Neurodegenerative Disease
Research Information
Research Interests
Neurodegenerative disease, microbiome, immunity, stem cell biology
Research Projects
The Burberry group is broadly interested in understanding how the immune system interacts with the nervous system and our environment to support neuronal homeostasis. In the past decade, genome wide association studies involving thousands of cases and controls and next generation sequencing studies of afflicted families have drastically expanded our knowledge of common genomic polymorphisms and rare mutations that confer risk to neurodegeneration. Intriguingly, many genes whose variation modifies neurological disease risk are enriched in cells of the immune system, including microglia. While our efforts have shed light on an important role for the microbiome in shaping an individual’s propensity of developing ALS/FTD, the precise inputs through which the environment stimulates the immune system to change brain health remain poorly understood. Our goal is to uncover the circuits, cell types and pathways in which these disease-associated perturbations function with the hope that with time, our discoveries will ultimately be leveraged to improve patient care.
Recent Funding
NIH/NIA R00
Publications
C9ORF72 Suppresses Systemic and Neural Inflammation Induced by Gut Bacteria, Nature, 2020