Scientists / Our Scientists

Jesse Hanson

Senior Principal Scientist, Neuroscience, Research Biology

Postdoc Mentor

"I’m excited for the opportunity to discover new aspects of disease biology and then translate that insight into therapeutic approaches."

Years at Genentech

Since joining Genentech, I’ve engaged in research aimed at understanding the basis of neural circuit dysfunction in diseases such as Alzheimer’s. Based on this research, my lab has pursued therapeutic approaches for modulating synapse function. A more recent focus of my lab is to understand the interaction of glial cells with neurons during disease pathogenesis. While glial cell activation can have aspects that are beneficial in the diseased brain, current projects focus on identifying the pathways that mediate damaging attack on neurons by activated glial cells. This research is identifying potential points of therapeutic intervention for protecting against the harmful aspects of neuroinflammation.

Postdoctoral Mentor

The Genentech postdoc program provides a unique opportunity to pursue fundamental research, much as in a well-resourced academic setting, while at the same time being immersed in a cutting-edge drug discovery environment. Projects in my lab focus on using the latest tools to uncover new insight into the neurobiology of disease.

Featured Publication

Complement C1q-dependent excitatory and inhibitory synapse elimination by astrocytes and microglia in Alzheimer's disease mouse models.

Nature Aging. 2022 Sep;2(9):837-850

Dejanovic B, Wu T, Tsai MC, Graykowski D, Gandham VD, Rose CM, Bakalarski CE, Ngu H, Wang Y, Pandey S, Rezzonico MG, Friedman BA, Edmonds R, De Mazière A, Rakosi-Schmidt R, Singh T, Klumperman J, Foreman O, Chang MC, Xie L, Sheng M, Hanson JE.

View Abstract

GluN2A NMDA Receptor Enhancement Improves Brain Oscillations, Synchrony, and Cognitive Functions in Dravet Syndrome and Alzheimer's Disease Models.

Cell Rep. 2020 Jan 14;30(2):381-396.e4.

Hanson JE, Ma K, Elstrott J, Weber M, Saillet S, Khan AS, Simms J, Liu B, Kim TA, Yu GQ, Chen Y, Wang TM, Jiang Z, Liederer BM, Deshmukh G, Solanoy H, Chan C, Sellers BD, Volgraf M, Schwarz JB, Hackos DH, Weimer RM, Sheng M, Gill TM, Scearce-Levie K, Palop JJ.

View Abstract

Complement C3 Is Activated in Human AD Brain and Is Required for Neurodegeneration in Mouse Models of Amyloidosis and Tauopathy.

Cell Rep. 2019 Aug 20;28(8):2111-2123.e6.

Wu T, Dejanovic B, Gandham VD, Gogineni A, Edmonds R, Schauer S, Srinivasan K, Huntley MA, Wang Y, Wang TM, Hedehus M, Barck KH, Stark M, Ngu H, Foreman O, Meilandt WJ, Elstrott J, Chang MC, Hansen DV, Carano RAD, Sheng M, Hanson JE.

View Abstract

Changes in the Synaptic Proteome in Tauopathy and Rescue of Tau-Induced Synapse Loss by C1q Antibodies.

Neuron. 2018 Dec 19;100(6):1322-1336.e7.

Dejanovic B, Huntley MA, De Mazière A, Meilandt WJ, Wu T, Srinivasan K, Jiang Z, Gandham V, Friedman BA, Ngu H, Foreman O, Carano RAD, Chih B, Klumperman J, Bakalarski C, Hanson JE, Sheng M.

View Abstract

Positive Allosteric Modulators of GluN2A-Containing NMDARs with Distinct Modes of Action and Impacts on Circuit Function.

Neuron. 2016 Mar 2;89(5):983-99.

Hackos DH, Lupardus PJ, Grand T, Chen Y, Wang TM, Reynen P, Gustafson A, Wallweber HJ, Volgraf M, Sellers BD, Schwarz JB, Paoletti P, Sheng M, Zhou Q, Hanson JE.

View Abstract

A current focus of my group is understanding the role of the immune response in the central nervous system during neurodegeneration. We are particularly interested in how activated microglia and astrocytes interact with neural circuits and which pathways could be targeted for neuronal protection.

Emory University, PhD in Neuroscience – 2003
University of California, BS in Physiology and Neuroscience – 1997

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Jesse Hanson

Senior Principal Scientist, Neuroscience, Research Biology

Postdoctoral Mentor

Featured Publication

Complement C1q-dependent excitatory and inhibitory synapse elimination by astrocytes and microglia in Alzheimer's disease mouse models.

GluN2A NMDA Receptor Enhancement Improves Brain Oscillations, Synchrony, and Cognitive Functions in Dravet Syndrome and Alzheimer's Disease Models.

Complement C3 Is Activated in Human AD Brain and Is Required for Neurodegeneration in Mouse Models of Amyloidosis and Tauopathy.

Changes in the Synaptic Proteome in Tauopathy and Rescue of Tau-Induced Synapse Loss by C1q Antibodies.

Positive Allosteric Modulators of GluN2A-Containing NMDARs with Distinct Modes of Action and Impacts on Circuit Function.