Mahru came to the Buck Institute with a broad background in cellular and molecular biology, having studied HIV and influenza viruses at the University of Washington before moving to UC San Diego where he received a Ph.D. for work studying molecular mechanisms governing synapse development in mice. In joining Dr. Ellerby’s lab at the Buck, he seeks to apply his experience in these fields towards a better understanding of therapeutic approaches to Huntington’s Disease. One primary approach applies ongoing advances in stem cell biology to develop patient-specific pluripotent cells as a tool for studying the mechanisms of Huntington’s Disease pathology, as well as a potential avenue for cell replacement therapeutics in neurodegenerative diseases such as Huntington’s Disease.

Francesco De Giacomo received his BS in Molecular Cell Biology with a minor in Chemistry from Dominican University of California. Francesco’s work in the Ellerby lab has consisted of characterizing new fragment mouse models of Huntington’s disease, novel caspase-6 inhibitors and neo-epitope antibodies to caspase cleavage sites of huntingtin. Francesco currently helps manage multiple projects for the Ellerby lab that look at the systems biology, proximal events and bioinformatics analysis of Huntington’s disease.

Bachir graduated from UC Berkeley with a major in Molecular Cell Biology with emphasis in Neurobiology. As a George Miller Scholar, he conducted research on Alzheimer’s disease at UC Berkeley, where he observed changes on Beta Amyloid protein levels by using dominant negative mutation on VPS4 A, and VPS4B. At the Alzheimer’s Service of the East Bay, he worked with patients to better his understanding of the impact of the disease in different stages firsthand. At the Buck Institute, he is currently working on neurogenesis using a combination of growth factors in Huntington’s disease for his master’s degree.

Jennifer's work primarily focuses on the development of novel targets for the treatment of Huntington’s disease using an array of cell, murine and post mortem human tissue in neurodegenerative disease models. She screens the Druggable Genome siRNA library to identify novel targets that modulate mutant huntingtin toxicity. Once targets have been identified, small molecule inhibitors are tested in cell-based models and advanced to animal models if shown to be efficacious. A unique protein identified in our screen was published in Neuron, titled "Matrix Metalloproteinases are modifiers of Huntingtin Proteolysis and Toxicity in Huntington Disease."

Robert O'Brien received his BS in Biological Sciences from the University of Vermont, where his undergraduate research training focused on forward and reverse genetic techniques to study the symbiotic relationship between legumes and the soil bacterium Rhizobium. He received his PhD from the University of California, San Diego, where he used mass spectrometry to study post-translational regulation of proteins in embryonic stem cells.

His work in the Ellerby Lab focuses on understanding the role that post-translational modifications of the protein that causes Huntington's Disease (huntingtin) play in the toxicity of the protein. Specifically, examining interactions of caspase cleavage products of huntingtin in mouse models of HD and the role of acetylation in the turnover of huntingtin in cell culture-based models of the disease.

I have had a strong interest in neuroscience very early in my studies. After pursuing a masters degree at the International Max Planck Research School in Tübingen, Germany and an internship at University of California, Irvine, I decided to focus on stem cell research during my PhD at the University of Connecticut. My work emphasized understanding the differentiation mechanisms of stem cell populations towards a dopaminergic phenotype. Currently I am involved in a study testing a compound with beneficial effects for a mouse model of Huntington’s disease, which might be a candidate in future therapeutic drug trials. Our goal is to optimize the structure of the compound and dissect its mechanistic action, which will ultimately allow us to identify the downstream targets and useful clues for Huntington’s disease pathogenesis. In addition, I am studying the role of FOXO, a molecule regulating lifespan, in the context of spinocerebellar ataxia 7. Understanding more about longevity pathways is vital, since they might harbor the key to preventing neurodegenerative disorders. With a battery of gain and loss of function experiments, I found changing levels of FOXO promotes degradation or accumulation of ataxin-7 and toxicity in an in vitro cerebellar model of spinocerebellar ataxia.

Khan received his masters in toxicology and PhD in neurotoxicology at Hamdard University, New Delhi. During his Masters, he studied neurobehavioral toxicity of organophosphates and surveyed bangle industries. His interest in understanding and treating neurodegenerative diseases led him to study neuroprotection in a 6-OHDA model of Parkinson's disease during his PhD. Later at UCD, he studied dopamine metabolism and its toxicity in dopminergic neurons. Currently, Dr Zafar's research focuses on genetic modulation of adult stem cells, understanding the proteolysis of Htt in Huntington Disease and carrying out preclinical therapeutic studies in HD.

Ningzhe received a Ph.D. degree from University of Rochester where he studied function and development of glial cells and their progenitors in rodent central nervous systems. After joining Dr. Ellerby’s lab at Buck in 2008, he continued the study in neuroscience with a focus on the neurodegenerative disease: Huntington’s disease (HD). He is using multiple systems, including animal models and cell models, to uncover disease mechanisms and to search for potential therapies for HD. One important part is to utilize human induced pluripotent stem cells to model the disease, make genetic correction and eventually replace cells lost in HD.