As a part of the German Institute for Dementia Prevention (DIDP), the Saarland University, and the Institute for experimental Neurology we are interested in the molecular biochemical process during aging and dementia, in particular Alzheimer‘s disease.
Alzheimer‘s disease (AD) is a devastating neurodegenerative disorder; the pathology is characterized by extracellular senile plaques, mainly consisting of beta-amyloid (Abeta), a 40-42 amino acid long peptide. Abeta is generated by sequential proteolytic cleavage of the amyloid precursor protein (APP) involving beta- and gamma-secretase.
Impaired physiological function of specific proteins is a common cause of disease, therefore knowledge of the physiological function of APP is important to understand AD and is one of our major goals. We are using interdisciplinary approaches ranging from biochemistry, bioanalytics, biophysics, bioinformatics and cellular and molecular biology to in vivo and in vitro models to elucidate these molecular mechanisms.
In our previous work we showed that APP-processing regulates lipid homeostasis. Disease relevance of this finding is highlighted by recent discovery of approx. one dozen AD-risk genes, the majority of which are lipid/lipid-related genes.
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