Appointments

• Assistant Professor of Pharmaceutical Sciences
• Graduate Faculty II, College of Graduate Studies

Bio

My lab is interested in understanding the cellular and molecular mechanisms contributing to the inflammatory environment in the Alzheimer’s disease brain.

Educational Background

• Ph.D. in Neuroscience, Case Western Reserve University, Cleveland, 2010
• B.A. in Biology, Colby College, Waterville, Maine, 2003

Courses

• Immunology & Biotechnology

Awards

• Post-doctoral National Research Service Award
• Pre-doctoral National Research Service Award
• Alzheimer’s Disease Research grant from the BrightFocus Foundation
• 2021 Innovation in Teaching Award, College of Pharmacy

Publications

See all my publications on Google Scholar.

• E.G. Reed-Geaghan, Q.W. Reed, P.E. Cramer, G.E. Landreth. Deletion of CD14 attenuates Alzheimer’s disease pathology by influencing the brain’s inflammatory milieu. J Neurosci 30:15369 (2010).
• E.G. Reed-Geaghan, J.C. Savage, A.G. Hise, G.E. Landreth. CD14 and Toll-like receptors 2 and 4 are required for fAβ-stimulated microglial activation. J Neurosci 29:11982 (2009).
• B.T. Casali, E.G. Reed-Geaghan. Microglial function and regulation during development, homeostasis and Alzheimer’s disease. Cells 10:957 (2021).
• B.T. Casali, K.P. MacPherson, E.G. Reed-Geaghan, G.E. Landreth. Microglial depletion rapidly and reversibly alters amyloid pathology by modification of plaque compaction and morphologies. Neurobiology of Disease 142:104956 (2020).
• E.G. Reed-Geaghan, G.E. Landreth. Plaque-associated myeloid cells derive exclusively from resident microglia in Alzheimer’s disease. J Exp Med 217: e20191374 (2020).