Beth Stevens

Beth Stevens, PhD

Research Associate in Neurology, Boston Children's Hospital; Investigator, Howard Hughes Medical Institute; Associate Professor of Neurology, Harvard Medical School.

Research Focus

Neuron-glia signaling, synapse development, plasticity.

Brief Research Description

The research in the Stevens laboratory is devoted to understanding the mechanisms by which neuron-glia and neural immune interactions facilitate the formation, elimination, and plasticity of synapses in heath and disease. In particular, the lab is focused on the role of microglia and the classical complement cascade in synaptic pruning and circuit refinement using a combination of molecular, electrophysiological, biochemical, and high-resolution imaging approaches in several model systems. A deep understanding of the mechanisms by which these pruning pathways are regulated and dysregulated in the developing brain could provide new insight into novel biomarkers and therapies in neuropsychiatric, neurodegenerative, and other brain diseases.

Key Publications (PMCIDs)

Single-Cell RNA Sequencing of Microglia throughout the Mouse Lifespan and in the Injured Brain Reveals Complex Cell-State Changes.
Hammond TR, Dufort C, Dissing-Olesen L, Giera S, Young A, Wysoker A, Walker AJ, Gergits F, Segel M, Nemesh J, Marsh SE, Saunders A, Macosko E, Ginhoux F, Chen J, Franklin RJM, Piao X, McCarroll SA, Stevens B.
Immunity 2019;50(1):253-71 e6. PMCID: PMC6655561

CD47 Protects Synapses from Excess Microglia-Mediated Pruning during Development.
Lehrman EK, Wilton DK, Litvina EY, Welsh CA, Chang ST, Frouin A, Walker AJ, Heller MD, Umemori H, Chen C, Stevens B.
Neuron 2018;100(1):120-34 e6. PMCID: PMC6314207

Complement and microglia mediate early synapse loss in Alzheimer mouse models.
Hong S, Beja-Glasser VF, Nfonoyim BM, Frouin A, Li S, Ramakrishnan S, Merry KM, Shi Q, Rosenthal A, Barres BA, Lemere CA, Selkoe DJ, Stevens B.
Science 2016;352(6286):712-6. PMCID: PMC5094372

Microglia contribute to circuit defects in Mecp2 null mice independent of microglia-specific loss of Mecp2 expression.
Schafer DP, Heller CT, Gunner G, Heller M, Gordon C, Hammond T, Wolf Y, Jung S, Stevens B.
Elife 2016;5:e15224. PMCID: PMC4961457

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