| Job Summary:
Exosomes from Adipose-derived Stem Cells Modulate Age-dependent Progression of Tauopathies: NIH funded postdoctoral positions are available immediately to highly motivated individuals to participate in ongoing studies on Alzheimer's disease (AD). Our laboratory is focusing on the idea that changes in immune function that occur with aging is an important factor to examine when following the progression of Tauopathies associated with Alzheimer’s disease and related disorders. Our lab focuses on examining the complex proteomic and functional phenotype of microglia and how this is affected by aging using mouse models of tauopathies. Furthermore, we have discovered that exosomes derived from adipose derived stem cells are potent modulators of inflammation and have potential to serve as therapeutic interventions in age-related tauopathies.
Job Duties:
Within the predetermined research scope and methodology, conduct research experiments in the field of Alzheimer’s disease to include: - Performing surgeries to create AD models
- Running behavioral analysis of animals
- Isolation of microglia
- Assay microglia in culture and using proteomics
- Assess brain pathology using immunohistochemistry
Collect and analyze data, including periodical/literature search and utilizing specialized skills in related field to analyze the collected data.
Participate/assist in manuscript writing for publication in scientific journals and/or presentations. May also assist in grant writing.
Lab maintenance, including equipment maintenance, and ordering of supplies as needed.
Other duties as assigned, which may include attending Scientific Conferences and Meetings.
Relevant publications:
Flowers A, Bell-Temin H, Jalloh A, Stevens SM, Jr., Bickford PC (2017) Proteomic anaysis of aged microglia: shifts in transcription, bioenergetics, and nutrient response. J Neuroinflammation 14:96.
Nash KR, Lee DC, Hunt JB, Jr., Morganti JM, Selenica ML, Moran P, Reid P, Brownlow M, Guang-Yu Yang C, Savalia M, Gemma C, Bickford PC, Gordon MN, Morgan D
(2013) Fractalkine overexpression suppresses tau pathology in a mouse model of tauopathy. Neurobiol Aging 34:1540-1548.
Patel NA, Moss LD, Lee J-Y, Tajiri N, Acosta S, Hudson C, Parag S, Cooper DR, Borlongan CV, Bickford PC (2018) Long noncoding RNA MALAT1 in exosomes drives regenerative function and modulates inflammation-linked networks following traumatic brain injury. Journal of Neuroinflammation 15:204.
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