Academic Title(s)

• Assistant Professor of Pharmaceutical Sciences

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).