The Team
The neuroscience faculty at Penn is a large, talented, and diverse group including more than 150 individuals, spanning 32 departments in 5 schools. The training program formally includes 20 of these faculty but special accommodations can be made for candidates for admission desiring to work with other Penn faculty whose work encompasses other components or the ReConNecT-IT program.
Program Directors
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Read More about Frances Jensen, MDFrances Jensen, MD
Chair, Department of Neurology, Co-Director Penn Medicine Translational Neuroscience Center Perelman School of Medicine at the University of Pennsylvania
Frances Jensen, MD
Chair, Department of Neurology, Co-Director Penn Medicine Translational Neuroscience Center Perelman School of Medicine at the University of Pennsylvania
Dr. Jensen is Professor of Neurology and Chair of Neurology at the PSOM and Co-Director of the Penn Medicine Translational Neuroscience Center. She was formerly Professor of Neurology, Harvard Medical School (HMS) and Director of Translational Neuroscience and Director of Epilepsy Research at Boston Children's Hospital. Her research focuses on mechanisms of epilepsy and stroke, with specific emphasis on injury in the developing brain and the synaptic and circuit changes associated with brain injuries and recovery from injuries. One specific translational outcome from her laboratory investigations of neonatal injury has been translated into the development of age-specific therapies for clinical trial development.
Dr. Jensen was nominated to the National Academy of Medicine (NAM) in 2015. She received a 2007 Director’s Pioneer Award from the NIH to explore the interaction between epileptogenesis and cognitive dysfunction and the 2008 American Epilepsy Society Basic Science Research Award. Dr. Jensen also sponsored an FDA-approved IND for an ongoing multi-center clinical trial of a novel therapy for neonatal seizures, generated from basic research in her laboratory. Major leadership positions held by Dr. Jensen include President of the American Epilepsy Society in 2012; she has also served on a number of other leadership boards including the Council for the Society for Neuroscience, the nominating committee at the American Neurological Association, and Council at NICHD. She is currently a member of the Health Sciences Policy Committee at NAM and on the BRAIN Initiative Multi-Council Working Group at NIH. Dr. Jensen is also an advocate for awareness of adolescent brain development, its unique strengths and vulnerabilities, and its impact on medical, social, and educational issues unique to teenagers and young adults. She has authored the New York Times bestseller entitled “The Teenage Brain”.
At Penn, in addition to her role as Chair of the Neurology department, Dr. Jensen is a member of the Neurology Residency Steering Committee, and a faculty member in the Neuroscience Graduate Group, the Pharmacological Science Graduate Group, and the Mahoney Institute of Neuroscience (MINS). She is also faculty on Penn’s R25.
You can learn more about Dr. Jensen here.
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Read More about Geoffrey Aguirre, MD, PhDGeoffrey Aguirre, MD, PhD
Professor of Neurology, Perelman School of Medicine at the University of Pennsylvania
Geoffrey Aguirre, MD, PhD
Professor of Neurology, Perelman School of Medicine at the University of Pennsylvania
You can learn more about Dr. Aguirre here.
Biostatistics Advisor
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Read More about Sharon Xie, PhDSharon Xie, PhD
Professor of Biostatistics and Epidemiology, Perelman School of Medicine at the University of Pennsylvania
Sharon Xie, PhD
Professor of Biostatistics and Epidemiology, Perelman School of Medicine at the University of Pennsylvania
Sharon Xiangwen Xie, PhD, is Professor of Biostatistics and a faculty member of the Department of Biotatistics and Epidemiology as well as a senior scholar in the Center for Clinical Epidemiology and Biostatistics. Dr. Xie’s statistical methodology research focuses on survival analysis, longitudinal analysis, measurement error problems, missing data, and receiver operating characteristic (ROC) analysis in response to methodological problems arising in her collaborative work in age related neurodegenerative diseases. She has developed new methods to reduce the biases of relative risk estimators in Cox regression models in the presence of covariate measurement error. She has also developed innovative methods to reduce bias in diagnostic evaluation measures for biomarkers with high variability (measurement error) and improve efficiency in survival analysis with uncertain endpoints using a validation subsample. These methodology developments have broad applications in age related neurodegenerative diseases.
Dr. Xie is an experienced mentor for supervising dissertation research in biostatistics. She has served as the dissertation advisor for multiple graduate students. Dr. Xie has also trained over 15 post-doctoral fellows in the neurosciences by serving as their biostatistics mentor, including three of the eight trainees appointed in the first cycle of this T32.
You can learn more about Dr. Xie here.
Advisory Committee Chair
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Read More about Marc Dichter, MD, PhDMarc Dichter, MD, PhD
Professor of Neurology (Emeritus), Perelman School of Medicine at the University of Pennsylvania
Marc Dichter, MD, PhD
Professor of Neurology (Emeritus), Perelman School of Medicine at the University of Pennsylvania
Dr. Dichter is Professor of Neurology and was Director of Mahoney Institute of Neuroscience (MINS) at Penn for 9 years and Director of the Penn Epilepsy Center for 20 years. He was Co-PI with Dr. Jensen for the first five years of this T32; this role is now being turned over to Dr. Alice Chen-Plotkin. Dr. Dichter will remain active as a mentor for our Fellows and to help supervise recruitment and monitoring the educational and scientific programs of our Fellows.
Dr. Dichter has supervised a major clinical program, and has been active in both basic neurobiological research and clinical research. He worked on new therapies for epilepsy and anti-epileptogenesis. He led pilot clinical trials testing methods for preventing epilepsy after traumatic brain injury (funded by the DOD) and after intracerebral hemorrhage (sponsored by UCB Pharma). He has supervised the training of 13 graduate students and 38 postdoctoral fellows (20 research, 18 clinical), most of whom now hold academic positions. Dr. Dichter’s research, although focused on epilepsy mechanisms, has also been in other areas relevant to the neurobiology of disease, including mechanisms of excitotoxicity (with Dr. Dennis Choi), ALS (with a Fellow, Dr. Robert Brown), neurovirology (PPG with Drs. Bernard Fields, Mark Greene and Howard Weiner), the effects of AIDS on the nervous system (PPG with Dr. Dennis Kolson), mechanisms underlying autoimmune neurological disorders (NIH grant with Dr. Josep Dalmau) and biomarkers of AD pathology in patients with PD or mild cognitive impairment (Co-PI of a PA Tobacco Grant).
Dr. Dichter has been active in teaching the Neurobiology of Disease (NBD) to neurology residents, medical students, graduate students, and more recently, Penn undergraduate students, at Harvard Medical School and Penn, and via the Neurobiology of Disease Workshop (NDW) of the SFN. For many years, Dr. Dichter directed a graduate course in the Neurobiology of Disease (NBD) at Penn, and was the PI of an NIH Blueprint grant to develop a three-year curriculum in the NBD that was available on the web.
As Director of MINS, Dr. Dichter was responsible for overseeing the Neuroscience Graduate Group (~100 graduate students), and the Clinical Neuroscience Track program, an educational enrichment program for medical students planning an academic career in the clinical neurosciences. Dr. Dichter also initiated two campus-wide programs in translational neuroscience, establishing a program in cognitive neuroscience (initially funded by HHMI) and an innovative program in neuroengineering.
Advisory Committee
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Read More about John Detre, MD, PhDJohn Detre, MD, PhD
Professor of Neurology
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Read More about Wade Berrettini, MD, PhDWade Berrettini, MD, PhD
Professor of Psychiatry
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Read More about Brenda Banwell, MDBrenda Banwell, MD
Professor of Neurology (Child Neurology), Children’s Hospital of Philadelphia
Brenda Banwell, MD
Professor of Neurology (Child Neurology), Children’s Hospital of Philadelphia
You can learn more about Dr. Banwell here.
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Read More about Michael Robinson, PhDMichael Robinson, PhD
Professor of Pediatrics and Pharmacology, Children’s Hospital of Philadelphia
Michael Robinson, PhD
Professor of Pediatrics and Pharmacology, Children’s Hospital of Philadelphia
You can learn more about Dr. Robinson here.
Trainers
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Read More about Ishmail Abdus-Saboor, PhDIshmail Abdus-Saboor, PhD
Biology
Ishmail Abdus-Saboor, PhD
Biology
The nervous system is exquisitely tuned to mount the appropriate behavioral response to sensory stimuli ranging from a gentle caress to a harsh mechanical insult. How our nervous systems encode this information, from the level of sensory neuron activation in peripheral tissues up towards the central nervous system, in both normal and diseased states, remains enigmatic. Taking advantage of mouse molecular and genetic tools, the Abdus-Saboor lab is addressing important questions about pain sensory system perception – from the level of the gene to the level of organismal behavior.
You can learn more about Dr. Abdus-Saboor here.
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Read More about Stewart Anderson, MDStewart Anderson, MD
Psychiatry
Stewart Anderson, MD
Psychiatry
The focus of Anderson’s laboratory concerns the molecular and cellular mechanisms that govern the development of the mammalian forebrain in relation to neuropsychiatric disease. He uses mouse genetics, forebrain slice and dissociated culture techniques, as well as mouse and human embryonic stem cells in cell culture and transplantation experiments to study the development of the cerebral cortex. We are particularly focused on the fate determination of key subclasses of cortical inhibitory interneurons. Some current major projects in the lab include acceleration of the maturation for human stem cell derived neurons by reversible activation of mTOR signaling, the use of use of stem cell derived inhibitory interneurons transplants to correct circuit pathology and abnormal social behaviors in a mouse model of Dravet's syndrome autism, and mitochondrial deficits in iPS derived neurons from patients with schizophrenia and the 22q11 deletion syndrome
You can learn more about Dr. Anderson here.
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Read More about Amit Bar-Or, MDAmit Bar-Or, MD
Neurology
Amit Bar-Or, MD
Neurology
Bar-Or’s laboratory focuses on discovering underlying mechanisms for Multiple Sclerosis (MS) and related disorders in both adults and children. He runs a cellular and molecular neuroimmunology lab at Penn and CHOP with major research themes directed at understanding basic principles of immune regulation and immune-neural interaction, and their contribution to inflammation, injury and repair of the human central nervous system (CNS). Particular areas of focus have involved elucidation of antibody-independent mechanisms by which human B cells contribute to modulation of T cell and myeloid cell subsets and how these contribute to MS immune pathophysiology, studies of immune reconstitution biology, and mechanisms of neuro-immune interaction. A major translational paradigm that has yielded key discoveries in human autoimmune disease has been our integration of rigorously developed immune monitoring and imaging strategies to well-characterized patient cohorts prospectively followed in biological proof-of-principle therapeutic trials. These studies not only contribute to elucidating a therapy’s mode-of action, but also provide a unique window into human disease mechanisms, and development of clinically meaningful biomarkers as part of advancing precision medicine in autoimmune diseases.
You can learn more about Dr. Bar-Or here.
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Read More about Jean Bennett, MD, PhDJean Bennett, MD, PhD
Ophthalmology
Jean Bennett, MD, PhD
Ophthalmology
Research is focused on the identification and characterization of genes that are defective in untreatable hereditary retinal degenerations such as retinitis pigmentosa, macular degeneration and choroideremia and the use of targeted gene therapy to correct these disorders. We have also used retinal gene therapy to probe neural plasticity in the brain. Techniques: virus based delivery of functional genes into differentiated retinal cells. Our gene therapy clinical trial for congenital blindness was the first to enroll children for a non-lethal disease. Ultimately our gene therapy techniques may be employed for genetically induced neurodegeneration in other primary neurological disorders.
You can learn more about Dr. Bennett here.
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Read More about Nancy Bonini, PhDNancy Bonini, PhD
Biology
Nancy Bonini, PhD
Biology
The Bonini laboratory focuses on mechanisms of long term brain integrity. Launching from Drosophila, the laboratory studies the pathways of degeneration of various human disease genes, discovers new pathways involved, and extends these data to mammalian models and to human patient tissue. Recently, the laboratory focus has been on mechanisms of traumatic brain injury, mechanisms of stress pathways that are critical to protect from degeneration, gene toxicity associated with motor neuron disease and dementia, and epigenetic landscape of the aging and degenerating brain.
You can learn more about Dr. Bonini here.
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Read More about Beverly Davidson, PhDBeverly Davidson, PhD
Pediatrics, Pathology, and Laboratory Medicine
Beverly Davidson, PhD
Pediatrics, Pathology, and Laboratory Medicine
The Davidson laboratory is focused on inherited genetic diseases that cause central nervous system dysfunction, with a focus on (1) recessive, childhood onset neurodegenerative disease, in particular the lysosomal storage diseases such as the mucopolysaccharidoses and Battens disease; and (2) dominant genetic diseases; for example, the CAG repeat disorders, Huntington’s disease (HD) and spinal cerebellar ataxia, and (3), understanding how noncoding RNAs participate in neural development and neurodegenerative diseases processes. The research on childhood onset neurodegenerative diseases is focused on experiments to better understand the biochemistry and cell biology of proteins deficient in these disorders, and to develop gene and small molecule based medicines for therapy. In recent work, she demonstrated that the application of recombinant viral vectors to animal models of storage disease reversed CNS deficits. Therapies for dominant disorders are an exciting challenge and require that the dominant disease allele be silenced. To approach this, her laboratory developed reagents for expressing inhibitory RNA in vivo. This approach improved disease phenotypes in relevant models of dominantly inherited human neurodegenerative diseases. Her group was the first to show that gene silencing could improve disease symptoms in mouse models and more recently, in collaborative studies, showed that it was well tolerated in other animals. Her lab, along with colleagues experienced in gene-based medicine delivery to humans, are advancing these promising preclinical studies to clinical trials in HD patients. Her laboratory also investigates how naturally occurring noncoding RNAs, miRNAs, participate in cell fate decisions in normal development, and how their expression is altered in disease states. They found that miRNAs with altered expression in Huntington’s disease or spinocerebellar ataxia brains target proteins that themselves contribute to disease phenotypes. This work may reveal new targets for drug therapy. In development are also the tools to understand how miRNAs may participate in brain development using the mouse as a model organism.
You can learn more about Dr. Davidson here.
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Read More about Ramon Diaz-Arrastia, MD, PhDRamon Diaz-Arrastia, MD, PhD
Neurology
Ramon Diaz-Arrastia, MD, PhD
Neurology
Diaz-Arrastia’s laboratory is focused on identifying and validating prognostic and pharmacodynamic biomarkers of traumatic brain injury, with the goal of revolutionizing the design of future clinical trials of acute, subacute, and chronic traumatic brain injury. Their major focus presently is to use advanced neuroimaging methods to measure cerebral blood flow (CBF) and cerebrovascular reactivity (CVR) in patients during the acute, subacute, and chronic period after TBI. They were the first group to show that phosphodiesterase 5 (PDE5) inhibition reverses part of the deficit in CVR, and constitutes a promising therapy for traumatic cerebrovascular injury. They are also involved in identifying and validating novel molecular biomarkers that can be measured in blood, and have adopted ultra-sensitive immunoassays which allow measuring of brain proteins spilled at very low levels into the peripheral blood.
You can learn more about Dr. Diaz-Arrastia here.
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Read More about Joshua Dunaief, MD, PhDJoshua Dunaief, MD, PhD
Ophthalmology
Joshua Dunaief, MD, PhD
Ophthalmology
Age-related macular degeneration (AMD), the most common cause of blindness among people over 60 in the US, is thought to be caused or exacerbated by oxidative stress. Similar processes have been invoked in a variety of neurodegenerative disorders of the CNS. We have found elevated levels of iron in retinas from patients with AMD. Further, a mouse deficient in two iron export proteins develops retinal iron overload and retinal degeneration resembling AMD, as well as iron overload and degeneration of dopaminergic neurons in the substantia nigra. Iron can cause oxidative stress and has been associated with other age dependent neurodegenerations including AD and PD. Techniques: microarray analysis, histology and immunohistochemistry on post mortem human retinas and transgenic mouse retinas, retinal pigment epithelial cell tissue culture, the mouse photic injury model of retinal degeneration, and retinal gene therapy.
You can learn more about Dr. Dunaief here.
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Read More about Amelia Eisch, PhDAmelia Eisch, PhD
Anesthesia and Critical Care
Amelia Eisch, PhD
Anesthesia and Critical Care
Eisch’s laboratory focuses on how molecular, cellular, and circuit changes, particularly in the limbic system, influence cognitive and motivated behavior. She is specifically interested in how the hippocampal dentate gyrus is involved in both normal and pathological brain function with relevance to addiction and depression and developmental injuries. She has 20+ years developing the concepts and employing the technical and interpretational skills used in her lab’s research. Her early work detailed the neural mechanisms and circuitry underlying psychostimulant-induced dopaminergic toxicity, gaining experience working inside the brain’s classic “reward” circuitry and foundational knowledge on how to probe gene-function using behavioral metrics. Later, her interest in the brain reward pathway led “upstream” to the hippocampus which turned out to be a successful effort in finding novel factors or processes that contribute to or are influenced by motivated behavior, in this case, adult-generated hippocampal neurons. For example, she discovered the relationship among experimenter-delivered and self-administered-opiates, dentate gyrus neurogenesis, and the hypothalamic-pituitary-adrenal (HPA) stress axis.
You can learn more about Dr. Eisch here.
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Read More about Pedro Gonzalez-Alegre, MD, PhDPedro Gonzalez-Alegre, MD, PhD
Neurology
Pedro Gonzalez-Alegre, MD, PhD
Neurology
The lab’s long-range research goal is to develop treatments for human diseases caused by basal ganglia dysfunction, including inherited dystonia, spinocerebellar atazias, and Huntington’s disease. Laboratory research spans from the development of novel molecular therapeutic approaches in animal models to early-phase human trials. One specific objective of ongoing research in the laboratory is the identification of the neurobiological bases of dystonia and the development of therapeutic strategies for these and related incurable neurological disorders. The laboratory has initiated an ongoing project on therapeutic gene silencing for dystonia and the investigation on the biological function of the dystonia protein torsinA in the secretory pathway. The laboratory also expanded research to investigate the influence of the protein quality control processes and the role of regulatory RNA networks on dystonia pathogenesis. Furthermore, Dr. Gonzalez-Alegre also participates in several clinical research projects involving dystonia patients.
You can learn more about Dr. Gonzalez-Alegre here.
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Read More about Raquel Gur, MD, PhDRaquel Gur, MD, PhD
Psychiatry
Raquel Gur, MD, PhD
Psychiatry
The study of brain and behavior in psychosis across the lifespan has been the focus of Dr. Gur’s career. She has established and is leading the Penn Schizophrenia Research Center that conducts translational research integrating basic and clinical neuroscience. She has directed and participated in large collaborative studies where phenotypic measures including clinical, neurocognitive, and neuroimaging have been integrated with genomics. Current efforts focus on trying to obtain much needed information on the early precursors and initial phases of psychosis within a neurodevelopmental genomics framework. This approach requires large-scale studies that integrate brain-behavior phenotypic measures with genomics. Toward this goal, she has led collaborative projects that resulted in the identification of a large sample of psychosis-spectrum youths as well as an informative sample of patients with the neurogenetic disorder 22q11.2 Deletion Syndrome, which has a 25% increased risk for developing schizophrenia. Her research efforts have capitalized on progress in brain behavior phenotyping, genomics and computation in collaborations with Penn-CHOP investigators and globally. The Philadelphia Neurodevelopmental Cohort, shared publicly, is a product of such efforts. An important component of her academic mission is the training in research at all levels including undergraduates, graduate students, psychiatry residents, postdoctoral fellows and junior faculty.
You can learn more about Dr. Gur here.
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Read More about Erika Holzbaur, PhDErika Holzbaur, PhD
Physiology
Erika Holzbaur, PhD
Physiology
Research is focused on understanding the dynamics of motility along the cellular cytoskeleton driven by molecular motors, including cytoplasmic dynein and kinesin. This motility is required to drive active transport of vesicles and organelles along the axons and dendrites of the neuron. The lab is interested in dissecting the mechanisms leading to coordinated motor activity during vesicle transport. Previous work from the lab has shown that defects in motor function lead to neurodegenerative disease, and the group is now working to understand the mechanistic basis for this observation. The lab has a significant track record of contributions to the cellular and biophysical analysis of molecular motor function, combined with expertise in the mechanistic analysis of neurodegenerative disease.
You can learn more about Dr. Holzbaur here.
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Read More about Matthew Kayser, MD, PhDMatthew Kayser, MD, PhD
Psychiatry
Matthew Kayser, MD, PhD
Psychiatry
Dr. Kayser’s laboratory investigates the regulation and function of sleep during brain development. His work has established the fruit fly Drosophila as a powerful model for studying basic mechanisms of sleep neurobiology throughout the lifespan. He has defined circuits in the young adult fly brain that control sleep ontogeny, and ongoing efforts include large-scale screens to identify genes regulating sleep maturation during the juvenile critical period. His was also the first group to demonstrate a sleep state in Drosophila larvae. This platform has opened new avenues to study the genes and circuits regulating sleep at an early neurodevelopmental time period. Moreover, he is using this system to study how sleep and neurogenesis are coupled at a molecular level. Dr. Kayser also directs a Sleep Mental Health Clinic, where he treats patients at the intersection of sleep and psychiatry. This clinical work has led to translational research centered on improving our understanding of how sleep abnormalities contribute to psychiatric disease.
You can learn more about Dr. Kayser here.
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Read More about Dennis Kolson, MD, PhDDennis Kolson, MD, PhD
Neurology
Dennis Kolson, MD, PhD
Neurology
The Kolson laboratory is focused on mechanisms of human immunodeficiency virus type 1 (HIV-1)- and inflammation-induced central nervous system (CNS) neurodegeneration and neuronal responses to such injury. The goal is to identify check-points in cell stress pathways and cell survival pathways that can be targeted to alter disease course in diseases driven by neuroinflammation. Research is focused on in vitro cell culture models of neurodegeneration, analysis of autopsied human brain specimens from HIV-infected individuals, analysis of samples and data from human clinical HIV cohort studies, and studies of simian immunodeficiency virus (SIV)-infected rhesus macaques. Using unique vitro cell culture systems the lab identified a key macrophage regulator of neurotoxin production, the antioxidant response enzyme, heme oxygenase-1 (HO-1). This led to establishing a link between loss of HO-1 expression and the release of soluble neurotoxins, resulting in neurodegeneration. Analysis of autopsied brain tissue from HIV-infected individuals demonstrate remarkably low levels of HO-1 expression, which suggests a significant role for HO-1 dysregulation in HIV-mediated neurodegeneration in vivo. Therapeutic targeting of HO-1 and related neuroinflammation pathways in the SIV-infected rhesus macaque are underway now. Finally, using specimens derived from human cohorts of HIV-infected individuals, the lab has linked common genetic polymorphisms (GT dinucleotide repeats) in the HO-1 gene promoter with HIV-associated neurodegeneration and cognitive impairment. Thus, HO-1 deficiency could represent a novel risk factor for neuronal injury as well as a novel target for therapeutic intervention against HIV- and other inflammation-associated neurodegenerative diseases. Defining this potential is the overall goal of current and future research.
You can learn more about Dr. Kolson here.
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Read More about Brian Litt, MDBrian Litt, MD
Neurology
Brian Litt, MD
Neurology
The Litt laboratory translates neuroengineering research directly into patient care. We collaborate broadly across disciplines to invent, develop and test new technologies and apply them to basic and clinical research. Our multidisciplinary efforts span a variety of scientific and clinical areas, including brain- machine interfaces, functional neurosurgery, network and computational neuroscience, epilepsy, movement disorders, intra-operative and ICU monitoring, and a broad array of “brain network” disorders. New findings from our lab indicate that important biomarkers of epileptic networks exist at the sub-millimeter scale not recorded by standard clinical electrodes. We are creating technology capable of recording high-resolution activity from clinically relevant areas. The platform of this new generation of electrodes is composed of active, flexible, conformable and multiplexed electronics. We are also developing new approaches for surgical treatment of medically refractory epilepsy. High-bandwidth EEG to map High Frequency Oscillations (HFOs) and microseizures may better localize epileptic networks, and enable more effective surgery and antiepileptic device therapy. Our work in this area includes: using novel hardware to record high-bandwidth intracranial EEG (iEEG), unsupervised detection and classification of ictal patterns utilizing machine learning methods for detecting and mapping epilepsy biomarkers in huge (Terabyte) data streams generated by high resolution arrays, and development of algorithms for detecting seizures for an implanted human device.
You can learn more about Dr. Litt here.
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Read More about Timothy Lucas, MD, PhDTimothy Lucas, MD, PhD
Neurosurgery
Timothy Lucas, MD, PhD
Neurosurgery
Dr. Lucas directs the Translational Neuromodulation Laboratory (TNL) and Co- Directs the Center for Neuroengineering and Therapeutics (CNT) with Dr. Litt. Dr. Lucas’ clinical practice focuses on the surgical treatment of epilepsy, building upon fellowship training in brain mapping, epilepsy and functional neurosurgery. This work has led to the development of minimally invasive surgical approaches to the hippocampus. Dr. Lucas’ clinical research focuses on human BCI experiments and clinical trials. Dr. Lucas’ translational research is focused on restoration of function using implantable/wearable custom circuits that augment existing neural pathways. The latest system, the Penn Brain-Machine-Brain-Interface (PennBMBI), wirelessly links sensor nodes on the extremities to implantable brain electrodes for continuous, autonomous recurrent brain stimulation. . The laboratory also develops implantable medical devices to restore bi-directional communication between the brain and the body following spinal cord injury. The TNL is the only laboratory at the University of Pennsylvania with active experiments ranging from computational modeling, rodent feasibility testing, nonhuman primate experiments and human trials.
You can learn more about Dr. Lucas here.
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Read More about David Lynch, MD, PhDDavid Lynch, MD, PhD
Pediatrics
David Lynch, MD, PhD
Pediatrics
Dr Lynch’s lab focuses on the understanding of the disease Friedreich’s ataxia (FRDA), the most common form of hereditary ataxia in the United States and Europe. Symptoms typically begin between the ages of 5 and 15 years and worsen over time. The pathophysiology of FRDA reflects the deficiency of the protein frataxin. Reduced frataxin levels impair the function of mitochondrial iron-sulfur-cluster-containing enzymes and ability to produce ATP. Recently, amelioration of frataxin deficiency by gene therapy in mouse models of FRDA has produced impressive benefit in reversing the phenotype, providing an evidenced-based approach for treatment of FRDA patients. Dr Lynch’s lab focuses identification of translational biomarkers of disease, as well as defining the pathophysiology in the nervous system. Their resources include multiple mouse models, cellular models, and samples from humans. He is also involved in clinical trials to take the laboratory findings into the clinical domain. Another focus of the Lynch lab has been on the role of alterations in glutamatergic transmission that have been proposed to be involved in a variety of disorders including cerebral ischemia, secondary damage in neuronal trauma, neuronal damage from prolonged seizures, schizophrenia and autism. Many of these are mediated by calcium entry through a specific glutamate receptor, the N-methyl D-aspartate (NMDA) receptor. Much evidence indicates the presence of multiple types of NMDA receptors in the brain, and evidence from his laboratory suggests that different subtypes play different roles in physiological and excitotoxic processes. They are presently examining the role of receptors subtypes in immune mediated dysfunction in the brain, such as the novel disorder anti-NMDA receptor encephalitis. They are also examining the role of nicotinic receptors in glutamatergic development and how it relates to schizophrenia and autism.
You can learn more about Dr. Lynch here.
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Read More about David Raizen, MD, PhDDavid Raizen, MD, PhD
Neurology
David Raizen, MD, PhD
Neurology
Quiescent behavioral states are universal to the animal world with the most famous and mysterious of these being sleep. Despite the fact that we spend one third of our life sleeping, the core function of sleep remains a mystery and the molecular basis underlying sleep/wake regulation is poorly understood. This is critically important because many neurological and behavioral disorders are characterized as either primary sleep disorders or have major sleep disturbances as part of their phenotype. It is also well understood that even minor alterations in circadian rhythms and sleep have major adverse health consequences, and at the extremes, lack of sleep creates a major breakdown in both brain and body function. We use C. elegans as a model system as it offers many experimental advantages, including powerful genetic tools, a simple neuroanatomy, and a behavior that has many characteristics of sleep in other animals. We have identified new regulators of sleep-like behavior in C. elegans and are currently studying how these regulators function to regulate sleep.
You can learn more about Dr. Raizen here.
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Read More about Steven S. Scherer, MD, PhDSteven S. Scherer, MD, PhD
Neurology
Steven S. Scherer, MD, PhD
Neurology
The lab focuses on the pathogenesis of inherited diseases of myelinated axons. Depending on whether a given mutation affects PNS axons, CNS axons, or both, the clinical manifestations will be neuropathy (PNS axons), myelopathy (CNS axons), or both. We work on how mutations in GJB1 and GJC2, the genes that encode connexin32 and connexin47, cause inherited demyelinating diseases in humans (and in mice). We have shown that the connexin32 is localized in myelin sheaths, that myelin sheaths have functional gap junctions, and that many connexin32 mutants have abnormal trafficking. We are actively studying how connexin32 mutants cause demyelination, including the partner(s) of connexin32 and connexin47 in CNS glial cells. We also study the molecular organization of myelinated axons - the basis for saltatory conduction – in normal myelinated axons, as well as during demyelination and remyelination. These findings have important implications for restoring conduction in demyelinating diseases. Finally, we study how axon- Schwann cell interactions regulate the development and regeneration of peripheral nerve and the pathogenesis of peripheral neuropathy. Techniques: light, confocal, and electron microscopy, immunocytochemistry, creating and analyzing transgenic mice, Northern and Western blotting, microarray analysis of gene expression, Schwann cell culture, and transfecting cells.
You can learn more about Dr. Scherer here.