Professor for Human Biology and Human Genetics
- Division: Human Biology and Human Genetics
- Address: Erwin-Schrödinger-Straße/Geb. 13, D-67663 Kaiserslautern
- Room: 13-113.1
- Phone: +49(0)631 205 2106
- Fax: +49(0)631 205 3517
- Email: s.kins[at]biologie.uni-kl.de
- 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
Major 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, Stiftung Rheinland Pfalz für Innovation, Alzheimer Forschung Initiative (AFI) and Klaus Tschira Stiftung.