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Kins, Stefan

Professor
Department of Human Biology and Human Genetics
State Research Center for Optics and Material Sciences
United States of America

Biography

1996-1999 Dr. phil. nat., Max Planck Institut für Hirnforschung, Frankfurt 1999-2001 Postdoc, Department of Molecular Psychiatry, University of Zurich, Switzerland 2001-2003 Post Doc, ZMBH 2003-2006 Project Leader, ZMBH 2005 Habilitation, University of Heidelberg 2007-2008 Project Group Leader, ZMBH Since 2008 Professor for Human Biology and Human Genetics, Dept. Biology, University Kaiserslautern

Research Interest

Alzheimer Disease, APP function and transport Alzheimer disease (AD) is the most common disease in elderly people. It is characterized by a progressive loss of cognitive functions, resulting in dementia. The cognitive decline is associated with the loss of neurons, reduced synaptic density, and two characteristic pathological hallmarks: neurofibrillary tangles containing the microtubule associated protein tau and extracellular plaques mainly composed of the -amyloid peptide (A) derived from the amyloid precursor protein (APP). APP is essential for normal synaptic function and its processing, which strongly depends on the intraneuronal localization, plays a major role in the etiopathology of AD. Our research focuses on the neuronal function of the APP gene family and the molecular motor composition underlying its intracellular traffic in neurons. Thereby we are mainly interested in changes of APP transport and function while aging and its consequences for AD. Specifically our research is currently addressing the following aims, using proteomic, biochemical, immunocytochemical and video microscopic methods in different neuronal model systems: 1. We determine the molecular basis of anterograde and retrograde transport of APP, whereby we investigate specifically the underlying motor composition and the influence of intracellular ligands as well as the influence of neuronal aging. 2. We found that APP/APLPs function as cell adhesion molecules and investigate the resulting physiological and pathogenic consequences of APP/APLPs malfunction. Thanks for funding of our research to the DFG, Fritz Thyssen-Stiftung, Landesstiftung Baden Württemberg, Hans und Ilse Breuerstiftung, DAAD und Alzheimer Forschung Initiative (AFI).

Publications

  • Rusu P, Jansen A, Soba P, Kirsch J, Löwer A et al. (2007) Axonopathy in APP transgenic Drosophila depends on the NPTY motif and is paralleled by defects in synaptic plasticity, Eur. J. Neurosci 25: 1079-1086

  • Rusu P, Jansen A, Soba P, Kirsch J, Löwer A (2007) Axonopathy in APP transgenic Drosophila depends on the NPTY motif and is paralleled by defects in synaptic plasticity, Eur. J. Neurosci 25: 1079-1086.

  • Back S, Haas P, Tschäpe J-A, Gruebl T, Kirsch J, et al. (2007) In neurons APP can be transported independent of any sorting signal to the axonal and dendritic compartment. J. Neurosci. Res 25: 1079-1086.

  • Deboer SR, You Y, Szodorai A (2001) Conventional Kinesin holoenzymes are composed of heavy and light chain homodimers. Biochemistry 47: 4535-4543

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