was born in 1963 in the USA. After completing her B.A. in Psychology at the University of Southern California in
1985, she began her doctoral training in Neuroscience at Princeton University. She completed her Ph.D. in 1990. For her post-doctoral fellowship she changed to Stanford University. She became Assistant Professor at the California Institute of Technology (Caltech) in 1993, Associate Professor in 1999 and Full Professor in 2004. In 1997 Erin Schuman was appointed Investigator at the Howard Hughes Medical Institute (HHMI). In 2009, she became Director of the Department of Synaptic Plasticity at the Max Planck Institute for Brain Research.
Erin Schuman received several awards and grants, including the Pew Scholars Award, the Beckman Young Investigator Award, and an Alfred P. Sloan Fellowship. In 1995, she was named as the American Association of University Women’s Emerging Scholar.
Many of the most debilitating neurological disorders remain without cure. This is true of all of the major neurodegenerative diseases, including Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, and Amyotrophic Lateral Sclerosis. But recent insights from basic neurobiological studies, new investigative tools, cell type-specific studies, and human genetic data are all converging to stimulate new hypotheses and to provide a better understanding the molecular mechanisms of neurological disease. Renowned neurobiologists from around the world will gather at the Picower Institute’s Fall 2016 Symposium to present their latest research findings and discuss vulnerability in and basic underlying mechanisms associated with neurological disease, as well as molecular pathways that could potentially be targeted for therapeutic treatments.
The Ackerman Lab works to identify the genes, pathways and networks involved in the development of the central nervous system and the age-related death of neurons. Using forward genetics, we have identified genes that govern proper axonal guidance and neuronal migration. We have also discovered novel mechanisms underlying neurodegeneration using this same approach. We use a combination of genetic, cell biological and genomic approaches to investigate the molecular and cellular events that link these mutations to the corresponding phenotype.
Dr. Brown’s laboratory has focused on the identification of gene defects that elucidate the molecular pathogenesis of selected neuromuscular diseases including amyotrophic lateral sclerosis (ALS, also known as Lou Gehrig’s disease), muscular dystrophy, adrenoleukodystrophy, hereditary neuropathy and hyperkalemic periodic paralysis. Knowledge of theses disease genes has facilitated the creation of mouse and cell-based models of these disorders. In turn, these resources have allowed study of therapeutic strategies using conventional small molecule approaches and new modalities such as inhibitory RNAi.
Michael E. Greenberg
Mike Greenberg grew up in Brooklyn, New York, attended Wesleyan University in Connecticut and received his PhD from Rockefeller University in 1982. Following postdoctoral training with Dr. Edward Ziff at New York University Medical School, Dr. Greenberg moved to Harvard Medical School in 1986. He is currently the Nathan Marsh Pusey Professor of Neurobiology and Chair of the Department of Neurobiology at Harvard Medical School. Mike Greenberg’s research interests span a broad range of topics related to the development of the nervous system. His characterization of signaling networks that control brain development has provided new insight into how disruption of normal nervous system development leads to neurological disorders including mental retardation and autism. Dr. Greenberg has received a number of awards for his research. In 2003, he was elected to the American Academy of Arts and Sciences. He is the 2006 recipient of the A. Clifford Barger Award for Excellence in Mentoring-Harvard Medical School and the 3rd Annual Edward M. Scolnick Prize in Neuroscience. In 2008, he was elected to the National Academy of Science and received the J. Allyn Taylor International Prize in Medicine.
Myriam Heiman received her Ph.D. in Biology from the Johns Hopkins University and her postdoctoral training in the laboratory of Paul Greengard at the Rockefeller University. In 2011, she joined the Broad Institute, the Department of Brain and Cognitive Sciences, and the Picower Institute for Learning and Memory at MIT.
Richard I. Morimoto is the Bill and Gayle Cook Professor of Biology, Department of Molecular Biosciences, and Director of the Rice Institute for Biomedical Research at Northwestern University, Evanston, IL.
He holds a B.S. from the University of Illinois at Chicago, received a Ph.D. in Biology (laboratory of Professor Murray Rabinowitz) from the University of Chicago in 1978, and conducted postdoctoral research (laboratory of Professor Matthew Meselson) and was a Tutor in Biochemical Sciences at Harvard University in Cambridge, MA. In 1982, Morimoto joined the faculty of the Department of Biochemistry, Molecular Biology, and Cell Biology at Northwestern University in Evanston, IL. He served previously as the Chair of Biochemistry, Molecular Biology, and Cell Biology, the Dean of The Graduate School, and the Associate Provost of Graduate Education at Northwestern University.
Beth Stevens received her PhD in Neuroscience in 2003 from the University of Maryland, College Park and completed her postdoctoral fellowship at the Stanford University School of Medicine in 2008. She is a recipient of several awards including the Smith Family Award for Excellence in Biomedical Research, Dana Foundation Award (Brain and Immunoimaging), Ellison Medical Foundation New Scholar in Aging award, John Merck Scholar Program, and MacArthur Fellows Program.
D. James Surmeier
Dr. D. James Surmeier is the Nathan Smith Davis Professor and Chair of the Department of Physiology at the Feinberg School of Medicine at Northwestern University and Director of the Morris K. Udall Research Center of Research Excellence for Parkinson’s Disease at Northwestern University. Dr. Surmeier received his Ph.D. in Physiology and Biophysics from the University of Washington in 1983. He trained with leaders in the field of neurophysiology, including Dr. Arnold Towe, Dr. William Willis, and Dr. Stephen Kitai. In 1998, he moved to the Department of Physiology at Northwestern University and assumed his current position in 2001. Dr. Surmeier’s research program focuses on the basal ganglia – neural structures controlling movement and intimately involved in the pathophysiology of Parkinson’s disease. He has authored over 150 peer-reviewed publications in journals such as Science, Nature, Neuron, Nature Neuroscience and the Journal of Neuroscience. He has served in several advisory capacities to the National Institutes of Health, including chairing study sections for the National Institute of Neurological Disorders and Stroke (NINDS) and acting as a Councilor for NIAAA. He also serves on the scientific advisory boards of several private foundations and serves on a number of editorial boards, including Molecular and Cellular Neuroscience, Neuron and Current Opinion in Neurobiology. He was elected as a Fellow of the American Association for the Advancement of Science and has received many other scientific awards including the NARSAD Established Investigator award, the Riker Award, the Picower Foundation Award, and the Jacob Javits Neuroscience Investigator Award.
Li-Huei Tsai received her P.h.D degree from the University of Texas Southwestern Medical Center at Dallas. She then took postdoctoral training from Ed Harlow’s laboratory at Cold Spring Harbor laboratory and Massachusetts General Hospital. She joined the faculty in the Department of Pathology at Harvard Medical School in 1994 and was named an investigator of Howard Hughes Medical Institute in 1997. In 2006, she was appointed Professor in the Department of Brain and Cognitive Sciences, and joined the Picower Institute for Learning and Memory at MIT.
X. William Yang
Dr. X. William Yang received his undergraduate education at Yale University, obtaining combined B.S./M.S. degrees from the Department of Molecular Biophysics & Biochemistry (MB&B) in 1991. He did his master’s thesis research in the laboratory of Professor Joan A. Steitz. He then completed M.D./Ph.D. training at Rockefeller University (Ph.D., 1998) and Weill Medical College of Cornell University (M.D., 2000). During his Ph.D. thesis research under the mentorship of Dr. Nathaniel Heintz at Rockefeller University, William co-invented (with Nathaniel Heintz and Peter Model) a genetic technology to engineer Bacterial Artificial Chromosomes (BACs) and to generate transgenic animals.
William’s own laboratory, established at UCLA in 2002, has made significant contributions in the use of BAC transgenesis to model human neurodegenerative disorders including Huntington’s disease (HD), Huntington’s disease-like 2 (HDL2) and Parkinson’s disease (PD), and the use of such models to dissect disease mechanisms and identify therapeutic targets. The Yang lab has also developed novel tools to study neuronal cell-type-specific gene expression, and to decipherinvivo protein interaction networks. Finally, the Yang lab studies the role of basal ganglia circuitry in the generation of normal and pathological behaviors.
Dr. Yang is a recipient of Brain Disorder Award from the McKnight Foundation, a 2014 NIH BRAIN Initiative award, and serves on the scientific advisory board for the Hereditary Disease Foundation.
Dr. Youle received an A.B. degree from Albion College and his Ph.D. degree from the University of South Carolina where he worked on the protein toxin ricin. He joined the lab of David Neville at the National Institute of Mental Health for postdoctoral work on the engineering of new cell-type-specific protein toxins. He joined the Surgical Neurology Branch of NINDS in 1985 as a principal investigator where he has developed new treatment strategies for brain tumors. His lab is now exploring the molecular mechanisms of programmed cell death and engineering therapeutic proteins to regulate cell survival.
Dr. Rudolph Tanzi is a Professor of Neurology and holder of the Joseph P. and Rose F. Kennedy Endowed Chair in Neurology at Harvard University. At the Massachusetts General Hospital (MGH), Dr. Tanzi serves as the Vice-Chair of Neurology (Research) and Director of the Genetics and Aging Research Unit, which consists of eight laboratories investigating the genetic causes of Alzheimer’s disease.
Dr. Tanzi has been investigating the molecular and genetic basis of neurological disease since 1980, when he participated in the pioneering study that led to location of the Huntington’s disease gene, the first disease gene to be found by genetic linkage analysis. Since 1982, Dr. Tanzi has investigated the genetic causes of Alzheimer’s disease (AD). He co-discovered all three genes that cause early-onset familial AD, including the first familial AD gene, known as the amyloid β-protein (A4) precursor (APP), and the presenilin genes. In 1993, Dr. Tanzi discovered the gene responsible for the neurological disorder known as Wilson’s disease, and over the past 25 years, he has collaborated on studies identifying several other disease genes including those causing neurofibromatosis, amyotrophic lateral sclerosis, and autism.
Dr. Tanzi currently spearheads the Alzheimer’s Genome Project, which identified several other AD gene including CD33, which plays a role in modulating neuroinflammation in AD. This achievement was named one of the “Top Ten Medical Breakthroughs of 2008” by Time Magazine. In 1994, Dr. Tanzi discovered that the metals, zinc and copper are necessary for the formation of neurotoxic assemblies of the Aβ peptide, the main component of β-amyloid deposits in brains of AD patients. Based on this discovery, Dr. Tanzi developed the “Metal hypothesis of Alzheimer’s disease”, which has led to clinical trials for treating and preventing AD by targeting Aβ−metal interactions (Prana Biotechnology, LTD; co-founder). Dr. Tanzi is also developing a potent class of gamma secretase modulators for preventing and treating AD as well as therapies aimed at targeting the genes, CD33 and TREM2, to curb neuroinflammation in AD. In 2014, Dr. Tanzi, Dr. Se Hoon Choi, and Dr. Doo-Yeon Kim reported the first in vitro model recapitualting AD neuropathology and showing that beta-amyloid can induce neurofibrillary tangles using human stem cell-derived neural cultures grown in three-dimensional culture systems.
Dr. Tanzi is one of the ten most cited researchers in AD, having co-authored over 475 research articles. He is also listed by Thomson Reuter as one of the top 1% of researchers in the field of neuroscience. He is also a co-author the popular book “Decoding Darkness: The Search for the Genetic Causes of Alzheimer’s Disease”, the New York Times best seller, “Super Brain”, and “Super Genes”. Dr. Tanzi has received several awards for his work, including the two highest awards for Alzheimer’s disease research: The Metropolitan Life Foundation Award and The Potamkin Prize. He has also received the Reagan National Alzheimer’s Disease Research Award, an NIH MERIT Award, and the “Oneness of Humanity” Global Award, and the Rustum Roy Spirit Award. He is an AAAS Fellow and was included on the list of the “Harvard 100: Most Influential Alumni” of over 220,000 living alumni. In 2015 he was included on the TIME magazine list, “TIME 100 Most Influential People in the World”, and has been acknowledged by as one of the “World’s Most Influential Scientific Minds”, 2014” by Reuters-Thompson, and named one of the “Top 20 Translational Scientists, 2013” by Nature Biotechnology. He received the 2015 Smithsonian American Ingenuity Award, the highest honor for innovation and invention in the U.S.A. His invited honorary lectures include a Nobel Forum Lecture, Smithsonian Institution Distinguished Lecture, and the Society for Neuroscience Public Lecture. Dr. Tanzi is the Chairman of the Cure Alzheimer’s Fund Research Consortium and serves on over 40 editorial and scientific advisory boards.
A fundamental capacity of the mammalian cerebral cortex is to process information in a form conducive to encoding, storage and retrieval of memories.
A general organizational principle of cortical memory circuits states that these steps all require a precisely orchestrated spatio-temporal interaction among a large number of relatively uniform excitatory and a numerically fewer but richly diverse population of inhibitory and neuromodulatory circuit elements. However, a mechanistic understanding of how these circuit motifs interact during elementary steps of memory processing is lacking. The goal of Attila Losonczy’s laboratory is to study the functional anatomical organization of memory circuits in the rodent hippocampus and to provide a biophysically-based characterization of elementary memory processing and storage mechanisms present in individual neurons. Losonczy uses high-resolution optical and electrophysiological methods together with optogenetic manipulations of specified circuit motifs in vitro, to study how dynamic interactions among excitatory, inhibitory and neuromodulatory inputs in various subcellular domains of neurons underlie information processing and storage in the hippocampal circuit. To link these elementary computations to memory functions, Losonczy applies high-resolution functional imaging in awake mice in vivo. He plan to investigate numerous fundamental questions including: (i) the role of specific spatio-temporal patterns of inhibitory and neuromodulatory inputs in determining neuronal input-output transformations, (ii) the effect of local inhibition and global neuromodulation on the dynamics of subcellular integration and compartmentalization of inputs, and (iii) regulation of various forms of synaptic and intrinsic plasticity by inhibitory and neuromodulatory inputs in the hippocampus.