Northwestern University Feinberg School of Medicine has a postdoctoral position open in a cutting-edge laboratory that sits at the intersection of Immunology, Neuroscience, and Computational Biology. The laboratory is focused on the role of microglia in the etiology and evolution of traumatic brain injury (TBI) and TBI-associated neurodegeneration. The candidate will lead studies in the following areas: 1) microglia transcriptional response to TBI in our murine models of TBI and Alzheimer’s disease (AD); 2) mechanisms of immune modulating therapy on the anatomic, physiologic, and transcriptional response to TBI and TBI-associated neurodegeneration; 3) develop and characterize a model of mild TBI (concussion) for the long-term study of microglial gene expression and response to immune modulating therapy.
Candidates must be highly self-motivated and self-sufficient with PhD or MD. A strong background in immunology and neuroscience is a requirement and experience with advanced flow cytometry, RNA sequencing and sequencing analysis is preferred. Experience with mouse models is a necessity. Competitive salary and benefit package.
Northwestern University is an Equal Opportunity, Affirmative Action Employer of all protected classes, including veterans and individuals with disabilities. Women, underrepresented racial and ethnic minorities, individuals with disabilities, and veterans are encouraged to apply. Hiring is contingent upon eligibility to work in the United States.
Internal Number: TBI012220
About Northwestern University
The CDC estimates nearly 2 million people sustain a traumatic brain injury (TBI) each year in the United States, contributing to over 30% of all injury related deaths. In fact, TBI related healthcare expenditures near 80 billion dollars annually with an average cost of 4 million dollars per person surviving a severe TBI. The impact of TBI is highlighted not only by its high mortality rate but also by the significant long-term complications suffered by its survivors with the progressive development of motor, cognitive, and behavioral disorders termed Chronic Traumatic Encephalopathy (CTE). Even subconcussive events, those resulting in subclinical brain dysfunction without the typical symptoms of concussion, may lead to long-term neurologic impairment. The immune response to TBI plays a fundamental role the development and progression of subsequent neurodegenerative disease and represents a complex interplay between peripheral innate immunity and the resident immune system of the injured brain—microglia. My laboratory is focused on shifting the existing paradigm of inflammatory and anti-inflammatory responses towards a cell-specific understanding of immune interaction between infiltrating monocytic cells and microglia.