Home Home Jennetta W. Hammond, Ph.D.

Jennetta W. Hammond, Ph.D.

Contact

Office (585) 273-2872

About Me
Credentials
Research
Publications

About Me

Faculty Appointments

Assistant Professor - Department of Neurology, Neuroimmunology (SMD)

Assistant Professor - Department of Neuroscience (SMD) - Joint

Credentials

Post-doctoral Training & Residency

University of Rochester Medical Center; Center for Neurotherapeutics Discovery. Advisor: Harris Gelbard 2012 - 2018

Education

PhD | University of Michigan. Cell and Developmental Biology. 2008

BS | Brigham Young University. Zoology. 2002

Research

My lab focuses on neuroimmune mechanisms that contribute to various neurological disorders. My current projects aim to understand the role of the Sez6 gene family. We have discovered that Sez6, Sez6L, and Sez6L2 are novel complement regulatory proteins that are primarily expressed in neurons. These complement inhibitors may serve as protective factors to preserve neurons and neuronal connections during critical windows in brain development when complement is engaged to prune away excess connections. These same complement inhibitors also appear to play a protective role in aging and could be very important in pathological conditions with heightened inflammation and complement activation like multiple sclerosis, traumatic brain injury, stroke, and Alzheimer’s.

My lab also studies Sez6L2 in the context of autoimmunity, as autoantibodies to Sez6L2 were recently discovered in multiple patients with semi-acute onset cerebellar ataxia. We have generated multiple mouse models of Sez6L2 autoimmune-mediated cerebellar ataxia in order to determine the pathological mechanisms involved. We are particularly interested in whether Sez6l2 autoantibodies are directly pathogenic or whether they are biomarkers of a cell mediated pathology.

Finally, my lab has a new project investigating the role of Mix23/ccdc58 in regulating mitochondrial stress pathways connected to movement disorders. This project began when we discovered a spontaneous mutation in the Mix23/ccdc58 gene was causing a late-onset ataxia phenotype in a subset of our Sez6L2 knockout mouse colony. We have since isolated the Mix23 mutation from our Sez6L2 knockout line. We have begun a thorough characterization of the ataxia phenotype and are investigating the molecular mechanisms by which loss or mutation of Mix23 leads to mitochondrial stress and neuronal dysfunction.

Publications

Journal Articles

Quantum Dots for Improved Single-Molecule Localization Microscopy.

Urban JM, Chiang W, Hammond JW, Cogan NMB, Litzburg A, Burke R, Stern HA, Gelbard HA, Nilsson BL, Krauss TD

The journal of physical chemistry. B. 2021 March 18125 (10):2566-2576. Epub 03/08/2021.

The Sez6 Family Inhibits Complement by Facilitating Factor I Cleavage of C3b and Accelerating the Decay of C3 Convertases.

Qiu WQ, Luo S, Ma SA, Saminathan P, Li H, Gunnersen JM, Gelbard HA, Hammond JW

Frontiers in immunology.. 2021 12 :607641. Epub 04/15/2021.

Survival and Motor Phenotypes in FVB C9-500 ALS/FTD BAC Transgenic Mice Reproduced by Multiple Labs.

Nguyen L, Laboissonniere LA, Guo S, Pilotto F, Scheidegger O, Oestmann A, Hammond JW, Li H, Hyysalo A, Peltola R, Pattamatta A, Zu T, Voutilainen MH, Gelbard HA, Saxena S, Ranum LPW

Neuron.. 2020 November 25108 (4):784-796.e3. Epub 10/05/2020.

Complement-dependent synapse loss and microgliosis in a mouse model of multiple sclerosis.

Hammond JW, Bellizzi MJ, Ware C, Qiu WQ, Saminathan P, Li H, Luo S, Ma SA, Li Y, Gelbard HA

Brain, behavior, and immunity.. 2020 July 87 :739-750. Epub 03/06/2020.

HIV Tat causes synapse loss in a mouse model of HIV-associated neurocognitive disorder that is independent of the classical complement cascade component C1q.

Hammond JW, Qiu WQ, Marker DF, Chamberlain JM, Greaves-Tunnell W, Bellizzi MJ, Lu SM, Gelbard HA

Glia.. 2018 December 66 (12):2563-2574. Epub 10/16/2018.

The Mixed-Lineage Kinase Inhibitor URMC-099 Protects Hippocampal Synapses in Experimental Autoimmune Encephalomyelitis.

Bellizzi MJ, Hammond JW, Li H, Gantz Marker, Marker DF, Freeman RS, Gelbard HA

eNeuro.. 2018 5 (6)Epub 12/03/2018.

Platelet Activating Factor Enhances Synaptic Vesicle Exocytosis Via PKC, Elevated Intracellular Calcium, and Modulation of Synapsin 1 Dynamics and Phosphorylation.

Hammond JW, Lu SM, Gelbard HA