The RTG joins scientists with expertise in basic, clinical and translational neuroscience to tackle Neurodevelopment and Vulnerability of the CNS from multiple angles to find novel interdisciplinary approaches.
Institute of Physiology and Pathophysiology
Chair of Physiology
- Phone number: +49 9131 8522295
- Email: firstname.lastname@example.org
- Website: http://www.physiologie1.uni-erlangen.de/en/alzheimer/index.shtml
1985 MD, LMU München
1987 Postdoctoral Fellow, LMU München
1991 Postdoctoral Fellow, University of Washington, Seattle, USA
1993 Group leader, LMU München
1996 Heisenberg Fellow, LMU München
2002 Professor of Phsyiology and Director, Institute of Physiology, Christian-Albrechts-Universität Kiel
2008 Professor of Physiology and Chairman, Institute of Physiology and Pathophysiology, Friedrich-Alexander-Universität Erlangen-Nürnberg
Our research focuses on the electric behavior of CNS neurons under normal and pathological conditions. Using high-resolution neurophysiologic and optical techniques, we investigate function and regulation of ion channels and synapses.
Our aim is to understand fundamental neural processes which are essential for cognitive and motor functions as well as for affective behavior and whose dysfunctions might give rise to neuropsychiatric disorders.
Role of the ASM/ceramide system in mediating vulnerability to neuropsychiatric disease
1988 PhD, Karl Franzens University, Graz, Austria
1988 Postdoctoral Fellow, Life Sciences Centre, Dalhousie University, Halifax, Canada
1992 Research Assistant, Department of Biology, University of Freiburg
1992 Max Planck Fellow, Max Planck Institute for Brain Research, Frankfurt/Main
1993 Research Group Leader, Max Planck Institute for Brain Research, Frankfurt/Main
1998 Heisenberg Fellow, Max Planck Institute for Brain Research, Frankfurt/Main
2004 Professor of Animal Physiology/ Neurobiology, Magdeburg, FAU Erlangen-Nürnberg
2006 Professor and Chair of Animal Physiology/ Neurobiology, FAU Erlangen-Nürnberg
The research of the Brandstätter and Regus-Leidig group focuses on molecules and mechanisms that play a role in the development and the structural and functional organization of chemical synapses in the CNS with a special focus on the retina. In our experimental approach, we combine methods ranging from immunocytochemistry and light- and electron microscopical imaging to biochemistry, cell and molecular biology, and electrophysiology.
As synaptophathies = malfunctioning synapses are a reason for many neurodegenerative diseases and neurological disorders, the aim of our research is to contribute to a better understanding of synapse function in health and disease.
Examining the synaptogenesis and synapse maintenance factor Bassoon as a putative factor for the differential sensitivity of photoreceptors to late-onset degeneration
2003 Dr. sc. nat. and PhD in Neuroscience, University of Zurich, Switzerland
2003 Fellow of Swiss National Foundation, Leibniz Institute of Neurobiology, Magdeburg
2005 Postdoctoral Fellow, Leibniz Institute of Neurobiology, Magdeburg
2009 Group Leader, Leibniz Institute of Neurobiology, Magdeburg
2013 Independant Junior Research Group Leader, Leibniz Institute of Neurobiology, Magdeburg
2016 Professor, FAU Erlangen-Nürnberg
My group is interested in the cellular and molecular mechanisms underlying plasticity of presynaptic function in healthy brain and in disease.
The project aims to further increase the understanding of the pathophyiological link between development and the pathogenesis of adult-onset neuropsychiatric and -degenerative disease by systematically investigating critical regulators of activity-dependent gene expression.
1985 MD, University of Ulm
1986 Postdoctoral Fellow, Department of Psychiatry, University of Würzburg
1989 Associate Professor of Psychiatry, University of Würzburg
1996 Associate Professor, Head of Gerontopsychiatric Unit, University of Göttingen
2000 Professor and Chair, Department of Psychiatry, Friedrich-Alexander-Universität Erlangen-Nürnberg
Our research focuses on sphingolipid metabolism and neuropsychiatric disorders, on the pathophysiology of major depressive disorder and Alzheimer’s disease and on the early and differential diagnosis of Alzheimer’s disease.
Role of the ASM/ceramide system in mediating vulnerability to neuropsychiatric disease
Institute of Anatomy and Cell Biology
- Phone number: +49 9131 85-22264
- Email: email@example.com
- Website: https://www.anatomie1.med.fau.de/mitarbeiter/stefanie-kuerten
2008 MD, University of Cologne and Case Western Reserve University, OH, USA
2011 Habilitation in Anatomy and Cell Biology, University of Cologne
2013 W2 professor at the Institute of Anatomy and Cell Biology, University of Würzburg
2015 Visiting professor at the Department of Neurology and Neurol. Sciences, Stanford School of Medicine, USA
2011 W3 professor and director at the Institute of Anatomy and Cell Biology, Friedrich-Alexander Universität Erlangen-Nürnberg
Multiple sclerosis (MS) is an autoimmune disorder of the central nervous system (CNS) and the most frequent neurological disease in young adults, leading to irreversible clinical deficits and premature retirement. On the one hand, my group focuses on the contribution of B cells and autoantibodies to the immunopathology of MS. Next to understanding the mechanisms of B cell-driven disease, we aim to develop novel therapeutic options and biomarkers for patients with MS. On the other hand, we are concerned with developing strategies to promote neuroregeneration and remyelination in the CNS.
The mechanisms behind the neuroprotective effect of the L-type calcium channel antagonist nimodipine in multiple sclerosis and its mouse model.
Institute of Biochemistry
Professorship of Molecular Medicine with focus on Molecular Imaging
- Phone number: +49 9131 8524622
- Email: firstname.lastname@example.org
- Website: http://www.biochem.fau.de/forschung/arbeitsgruppe.php?arbeitsgruppe=5
1998 MD, RWTH Aachen
1999 Postdoctoral Fellow, The Salk Institute for Biological Studies
2005 Group Leader, Helmholtz Center Munich
2011 Professor for Molecular Medicine and Molecular Imaging, Medical Faculty, Friedrich-Alexander Universität Erlangen-Nürnberg
Adult hippocampal neurogenesis – the generation of hippocampal neurons from stem cells throughout life – is a prime example of how the continuous activity of neurodevelopmental processes shapes plasticity of the adult brain. Notably, impaired adult neurogenesis is evolving as a major contributor to neuropsychiatric symptoms in ageing, mental and neurodegenerative diseases.
Research in my group aims to understand the molecular and cell biological mechanisms controlling adult hippocampal neurogenesis with a major focus on transcriptional and metabolic regulation.
Role of the intellectual disability and schizophrenia gene TCF4 in neural development and plasticity
Institute of Human Genetics
Chair of Human Genetics
- Phone number: +49 9131 8522020
- Email: email@example.com
- Website: http://www.humangenetik.uk-erlangen.de/forschung/arbeitsgruppen/index_ger.html
1986 MD, Universities of Göttingen und Lübeck
1986 Postdoctoral fellow, Inst. of Human Genetics, Univ. of Göttingen
1990 Group leader, Inst. of Human Genetics, Humboldt Univ. Berlin
1995 Founder and Project Leader, “Gene Mapping Centre” at Max-Delbrück-Center (MDC), Berlin
1998 Associate Professor, Humboldt Univ. Berlin
2000 Professor of Human Genetics at the FAU Erlangen-Nürnberg and Director of the Institute of Human Genetics at the University Hospital Erlangen
Genetic basis of neurocognitive disorders – the majority of these disorders, especially those with moderate to severe intellectual impairment, are caused by major genetic defects, but the genetic heterogeneity is extremely high, making their elucidation a challenge. In recent years, though, common pathways and cellular processes have emerged making identification of causative genes and the study of their pathophysiology an excellent avenue to understand cognition and eventually find treatments for affected individuals.
Research in my group aims to understand the genetic defects and molecular mechanisms controlling all process leading to disturbed cognition with a major focus on chromatin related processes of transcriptional control.
Identification of common pathways in intellectual disability and schizophrenia
1990 Dr. rer. nat., Julius-Maximilians-Universität Würzburg
1990 Postdoctoral Fellow, CMM, University of California at San Diego (UCSD)
1994 Group Leader, Centre for Molecular Neurobiology Hamburg (ZMNH)
2000 Chair of Biochemistry and Pathobiochemistry, Institute of Biochemistry, Friedrich-Alexander Universität Erlangen-Nürnberg
Myelination is a central function of glial cells in the vertebrate nervous system, and essential during development as well as in the adult as evident from the fact that myelination defects cause a variety of diseases that manifest at different times of life including leukodystrophies, autism spectrum disorders, schizophrenia, and multiple sclerosis.
Research in my group aims to understand the molecular mechanisms controlling gliogenesis, glial identity and homeostasis as well as myelination in the vertebrate central and peripheral nervous systems with a major focus on transcriptional regulation.
Role of the neurodevelopmental transcription factors Sox10 and Sox8 in myelin maintenance during adulthood
1986 M.D., School of Medicine, Albert-Ludwigs University, Freiburg and Louis-Pasteur University, Strasbourg (France)
1986 Residency in Neurology, Julius-Maximilians University Würzburg
1992 Postdoctoral fellow, Department of Neurosciences, University of California San Diego (UCSD) and McDonnell-Pew Center, Salk Institute, La Jolla
1995 Assistant Adjunct Professor of Neurosciences, UCSD
2002 Professor of Clinical Neurobiology, University of Regensburg
2008 Head of the Divison of Molecular Neurology and Movement Disorder Center, University Hospital Erlangen
2017 Member Governing Board, University Hospital Erlangen, and Vice Dean, Medical Faculty, FAU Erlangen-Nürnberg
The underlying molecular and cellular mechanisms in neurodegenerative diseases such as synucleinopathies are examined by using innovative translational neuroscience approaches in order to define the impact on the endogenous regenerative potential within the diseased brain, in particular the generation of new neurons and oligodendroglia. Furthermore, by taking advantage of our outpatient clinic we established human induced pluripotent stem cells and neural progeny for disease modelling purposes. The overall hypothesis is that impaired adult neuro- and oligodendrogenesis may contribute to distinct disease phenotypes. The present project investigates the functional consequences of alpha-synuclein pathology in oligodendrocytes with particular focus on myelin homeostasis.
Oligodendrogenesis and myelin homeostasis in alpha-synucleinopathies
1999 MD, Universities of Regensburg and Würzburg
2005 Specialist, Neurology, Universität Regensburg, Klinik und Poliklinik für Neurologie
2007 Humboldt Fellow, Research Associate, The Salk Institute for Biological Studies
2010 IZKF Junior Group Leader/ BMBF Research Group Leader Neuroscience, FAU Erlangen-Nürnberg
The overall goal of research in our laboratory is to model neurodegenerative diseases using stem cells. Specifically, we investigate neurodegeneration and regeneration in synucleinopathies including Parkinson’s disease and motor neuron diseases.
Impact of the hereditary spastic paraplegia gene SPG11 on neuronal development and maintenance
2003 MD, Friedrich-Alexander-University Erlangen-Nürnberg
2004 Clinical geneticist and research fellow, Institute of Human Genetics, FAU Erlangen-Nürnberg
2009 Guest Scientist, Radboud University Nijmegen
2009 Group leader, Institute of Human Genetics, FAU Erlangen-Nürnberg
2012 Specialisation in Human Genetics
2013 Habilitation in Human Genetics, FAU Erlangen-Nürnberg
Intellectual disability (ID) as a neurodevelopmental disorder is clinically and genetically extremely heterogeneous, and the number of underlying genes is still largely incomplete. Though recent studies have indicated that convergent molecular pathways underlie common phenotypic aspects, a comprehensive and systematic understanding of ID disorders and their underlying biology is still limited.
My group focuses on the clinical, genetic and functional characterization of ID disorders. Apart from phenotypic delineation of new disease entities, we aim to identify novel ID genes and to subsequently characterize their function and interaction with other ID genes/proteins in common pathways and networks.
Role of chromatin interacting and intellectual disability (ID) genes in neurodevelopment