Former Lab Members
Hanna was a postdoctoral fellow and trainee on the NIH/NINDS Training in Clinical and Basic Neuroscience (T32) Program during the COVID-19 pandemic (from June 2020 to April 2022). She investigated unconventional molecular mechanisms associated with neurodegenerative disorders, specifically tauopathies for which she was awarded a Michigan Alzheimer's Disease Research Center Pilot Award. Hanna transitioned to a Research Associate position in the Kanaan lab at Michigan State University - Grand Rapids Research Center and is continuing her passion for tau research.
Steph was a PhD candidate in the Neuroscience Graduate Program, and joined the Paulson lab in June of 2018 during which she investigated the role of the protein quality control protein, Ubiquilin-2, in synucleinopathies. She received her B.S. and M.S. degrees in Neuroscience from Brigham Young University where she studied the role of connexin-36 gap junction in reward. She is now pursuing a post-doctorate at UCSF at the Starr Lab.
Research Laboratory Specialist/Lab Manager
Sveta was a lab manager at the Paulson lab since August 2009. She also worked on different research projects studying neurodegenerative processes in the brain. She retired in January 2022.
Julia completed her doctoral studies in 2016 at the University of Texas Medical Branch where she studied tau oligomer structures in neurodegenerative disease and evaluated the efficacy of immunotherapy against oligomeric tau in mouse models. While at the Paulson lab, Julia investigated the role of protein quality control protein, UBQLN2, in regulating tau and other common aggregating proteins in neurodegenerative disease. She will be joining the NSF's Advancing Informal Science Learning Office as an AAAS Science Technology and Policy Fellow starting fall of 2021.
Dr. Moore successfully defended her thesis titled "Towards improved therapies, model systems, and understanding of Spinocerebellar Ataxia type 3" in May 2019. She began her graduate research in the Paulson Lab in 2014 focusing on the development of improved therapies and cell model systems for SCA3. She has published several manuscripts demonstrating the therapeutic potential of antisense oligonucleotide therapy targeting the ATXN3 transcript in SCA3 transgenic mice and SCA3 human cells lines. She also led the development and characterization of molecular phenotypes in a novel SCA3 human embryonic stem cell line for improved disease modeling. She completed an extended summer post-doc in the Paulson Lab and then moved to Chicago as Scientist, R&D Neurological Diseases, Exicure.
Hayley McLoughlin, PhD
Dr. Hayley McLoughlin is an Assistant Professor in the University of Michigan Neurology Department and Department of Human Genetics. She earned her Neuroscience doctoral degree in 2013 from the University of Iowa in Dr. Beverly Davidson's laboratory and completed a postdoctoral research fellowship under the guidance of Dr. Henry (Hank) Paulson at the University of Michigan. In her postdoc in the Paulson lab, she assessed the efficacy of antisense oligonucleotide therapy in mouse models of Spinocerebellar Ataxia type 3/Machado-Joseph disease (SCA3/MJD). In 2016, she took a research faculty position at the University of Michigan to lead gene therapy development for SCA3. In 2021, she was appointed to the tenure track in the Department of Neurology where her lab continues to focus on gene therapy for SCA3/MJD, as well as exploring potent biomarkers and mechanisms of neurodegenerative disease. Visit her lab website at https://sites.google.com/view/mcloughlinlab.
Biswa was a MD/PhD student who defended his thesis in 2015 in the Neuroscience Graduate Program. He explored the pathogenic mechanisms underlying SCA3, which is caused by an abnormal polyglutamine expansion in ataxin-3. His work sought to determine the mechanisms by which mutant ataxin-3 accumulates and aggregates in the brain, using a novel knock-in mouse model of SCA3. He also identified aberrant transcriptional changes that may contribute to toxicity in SCA3. He is currently a neuropathology resident at UCSF.
BBo Wang was a MD/PhD student who defended his Neuroscience Graduate PhD thesis in 2015. His dual degree is with Shanghai Jiao Tong University where he is now completing his medical degree work. Bo studied the in vivo function of Ube2W, an E2 ubiquitin conjugating enzyme that uniquely links ubiquitin to the amino-termini of proteins rather than to internal lysine residues. He generated and characterized Ube2W knockout mice, in the process establishing that this unusual E2 is important in a variety of tissues. He also explored the role of Ube2w in regulating the neurodegenerative disease protein in Huntington disease, Htt. He is currently a dermatology resident at the University of Michigan.
Phone: (734) 615-6156
Li was a postdoctoral fellow in the Paulson lab until 2014. Her research projects focused on 1) identifying the mechanism by which ataxin-3 modulates gene expression, 2) testing whether ataxin-3 modulates toxicity of a second polyQ disease protein, huntingtin, in a HD knock-in mouse model, and 3) defining the relationship between Ubiquilin 2 and polyglutamine disease proteins.
Phone: (734) 615-6156
Graham Atkin was a neuroscience graduate student who defended his PhD thesis in 2014. He studied the role of ubiquitin-proteasome pathways in handling the Alzheimer’s disease protein APP and in modulating synaptic plasticity. His thesis worked also focused on how the F-box adaptor subunit protein, Fbxo2, regulates activity-dependent receptor trafficking and expression in normal and pathological contexts. He is now an Assistant Professor at Michigan State University in Neuroscience and Anatomy.
K. Matthew Scaglione, PhD
The maintenance of proper protein quality control in the neuron is essential for proper neuronal function. Dr. Scaglione’s research involved identifying the mechanism that the protein quality control ubiquitin ligase CHIP (C-terminus of Hsc70-interacting protein) utilizes to facilitate the ubiquitination of chaperone bound substrates. Dr. Scaglione had a second project that focused on determining the biological role of specific ubiquitin chain linkages. Dr. Scaglione's work in the lab was funded in part by a K99 Pathway to Independence Award through the NIH. In August 2013, Matt began a tenure track assistant professorship at the Medical College of Wisconsin, Milwaukee, and in 2018 moved to join the faculty at Duke University, where he continues his work on ubiquitin pathways begun as a postdoctoral fellow in the Paulson lab.
Kai Chun Chen
Kai Chun is originally from Taiwan. She received her PhD in biochemistry with the focus on the biophysical properties of protein folding. Her projects in the Paulson Lab involved identifying the roles of ubiquilin-2 in the pathogenic mechanisms of Amyltrophic lateral sclerosis. She also worked on the SCA3 pathogenesis caused by the polyQ expansion in ataxin-3.
Katiuska Luna-Cancalon, PhD
Phone: (734) 615-5634
Dr. Luna-Cancalon was a postdoctoral fellow in the Paulson and Shakkottai labs. She received her PhD in Neuroscience at the Eberhard-Karls University Tuebingen, in Germany, where she focused on studying physiological changes in the motor system during learning and recovery of motor behavior after injury. Her research involved understanding neuronal dysfunction in two movement disorders, ataxia and dystonia. Her studies were based on the hypothesis that neurons in the cerebellum are key players in the progression of these disorders. Her goal was to characterize the physiological properties of these individual neurons in order to identify targets for pharmacological treatment. She is also interested in in vivo delivery therapies for ataxia. Dr. Luna-Cancalon now works as an academic advisor and counselor for the University.
Former Research Fellow
Eiko was a research fellow in the Paulson lab from 2011 to 2013. She received her MD from Kyoto University, Japan, in 2003. After completing her neurology residency, she joined the PhD program at Kyoto University Graduate School of Medicine in 2009, where she worked on generating a novel cell model of Parkinson's disease. She joined the Paulson lab in 2011 as a visiting researcher and then worked as a research fellow. Her main research interest lies in the mechanism and treatment of neurodegenerative diseases; her research at the Paulson lab focused on elucidating how multiple protein quality control systems are integrated and involved in the pathomechanism of neurodegenerative diseases through studying the function of ubiquilin-2, a causative gene of amyotrophic lateral sclerosis/frontotemporal lobar degeneration (ALS/FTLD). In August 2013, Eiko returned to Japan as a research fellow at Department of Degenerative Neurological Diseases, National Institute of Neuroscience, National Center of Neurology and Psychiatry. She continues to collaborate with the Paulson lab in the ubiquilin-2 research.
Wei Ling Tsou
Wei Ling was a neuroscience graduate student and PhD candidate at the National Yang Ming University in Taiwan. She joined the Paulson lab during the summer of 2008 to further her training in neurodegenerative disease. Her studies focused on the design and testing of RNAi as a therapy for Spinocerebellar Ataxia type 6 (SCA6). She also worked on determining whether disease-linked mRNA splice variants (/CACNA1A/) can be specifically targeted using shRNA-based RNAi systems. Wei Ling is now a postdoctoral fellow at Wayne State School of Medicine.
Ana Djarmati, PhD
Dr. Djarmati was a Fellow in the Paulson lab for two years, finishing in 2010. She holds a PhD in Molecular Biology and Biochemistry from the University of Belgrade, Serbia, and received part of her doctoral and initial postdoctoral training with Prof. Dr. Christine Klein at the University of Lübeck, Germany. While molecular genetics of movement disorders has been her main scientific interest, in the Paulson lab Dr. Djarmati directed her research toward functional studies of the Parkin protein, a ubiquitin ligase implicated in Parkinson's disease pathogenesis. Dr. Djarmati's research was funded by a German research fellowship. Dr. Djarmati returned to Germany where she is a Research Group Leader in the Institute of Neurogenetics at the University of Luebeck, Germany. Her email is email@example.com
Mary Y. Heng, PhD
After completing her neuroscience PhD thesis at UM, Dr. Heng performed a brief postdoctoral research fellow in the Paulson lab in 2008-2009. She continued work on a novel knock-in mouse model of Huntington disease in which she discovered early formation of microaggregates and early involvement of autophagic pathways in disease pathogenesis. Dr. Heng’s research during her postdoc also investigated the role of the protein quality control ubiquitin ligase, CHIP, in the normal aging brain and in Huntington Disease. After completing a postdoctoral fellowship at UCSF, Dr. Heng joined Akcea Therapeutics.
Edgardo Rodriguez, PhD
Dr. Rodriguez was a postdoctoral fellow in the lab from 2006 to 2010, focusing on the development of RNAi therapy for neurodegenerative diseases. In the lab, he designed and tested miRNA-based RNAi delivery systems in cell-based and animal models of Alzheimer’s disease, Spinocerebellar Ataxia type 3, and Spinocerebellar Ataxia type 6. These continuing projects are focused on improving the safety and efficacy of viral-based RNAi as potential therapy for various human neurodegenerative diseases. His work was funded in part by a training grant through the NIH. After his time in the Paulson laboratory, Dr. Rodriguez moved to the University of Iowa and then University of Florida as an Assistant Professor. Recently, he became the Chief Scientific Officer for a Lacerta Therapeutics.
Masayoshi Tada, MD, PhD
Dr. Tada was a research associate in the Paulson lab from 2008 to 2010, when he returned to his academic home, the Department of Neurology at Niigata University, Japan. Dr. Tada received his MD from Akita University in 1997, and his PhD in molecular neuroscience from Niigata University in 2007. In the Paulson lab, he created cell-based models to capture the earliest steps in oligomer formation by the polyglutamine disease protein, ATXN3. With these novel models, he then screened libraries of compounds to identify potentially useful compounds for preventive therapy in SCA3. Dr. Tada returned to Niigata in 2010 where he now is an Associate Professor in Neurology in the Brain Research Institute of Niigata University.
Sokol V. Todi, PhD
Originally from Tirana, Albania, Dr. Todi received a doctorate in Neuroscience at the University of Iowa, and finished his postdoctoral work with the Paulson lab in December 2010. His research in the lab focused on cellular properties and functional regulation of the polyglutamine disease protein, ATXN3. ATXN3 is a deubiquitinating enzyme, one member of a family of enzymes comprising almost 100 proteins in humans. Based on his findings that ATXN3 activity is carefully regulated in cells, Dr. Todi expanded his research to other deubiquitinating enzymes. Dr. Todi's work in the lab was funded by grants from the Nations Ataxia foundation and a K99 Pathway to Independence Award through the NIH. In 2010, Sokol joined the Pharmacology faculty at Wayne State University where he is now an associate professor. He continues the work begun as postdoctoral fellow and remains a collaborator with the Paulson lab.
MD-PhD Graduate Student
Aislinn was a neuroscience graduate student and MD/PhD trainee at the University of Iowa, who finished her thesis in Ann Arbor when the Paulson lab moved to the University of Michigan. As a student, she studied protein aggregation and protein quality control in mouse models of SCA3 (a.k.a Machado-Joseph disease). Aislinn's studies investigated how protein misfolding and aggregation contribute to neuronal dysfunction in neurodegenerative diseases. Aislinn successfully competed for a Predoctoral NRSA fellowship when performing her thesis work. After receiving her MD/PhD degrees in 2009, Dr. Williams completed Psychiatry residency at the University of Michigan, and joined the faculty at Iowa as an assistant professor in psychiatry and neuroscience.
The complexity of the ubiquitination pathways is emerging, and Brett studied how this complexity is regulated. In his thesis work, he determined that the neurodegenerative disease protein ataxin-3 is a deubiquitinating enzyme that edits topologically complex ubiquitin chains. His main project was to decipher the biochemical properties of ataxin-3, such as its ubiquitin binding and protease activities. Brett also worked to identify the role of ataxin-3 in the cell, especially relating to pathways of ubiquitin-dependent protein degradation.
Update: After Brett completed his PhD in cellular and molecular biology at Iowa in 2009, Brett became a Postdoctoral Research Associate at St. Jude Children’s Research Hospital in Memphis, Tennessee, working with J. Paul Taylor. His current e-mail address is firstname.lastname@example.org
Gautam Rajpal, PhD
Dr. Rajpal received his BA in Biology from the University of Pennsylvania and his PhD in Cell and Molecular Biology from the University of Michigan where he studied the process of insulin folding in pancreatic beta cells. Dr. Rajpal’s interest in protein folding led him to pursue neurodegenerative disease in which protein (mis)folding plays a prominent role. Dr. Rajpal is currently utilizing a high-throughput screen approach to identify inhibitors of Ataxin-3 aggregation, as well researching antisense oligonucleotide technology to treat SCA3.