Research Area A: Cellular Stress Signaling and Dysfunction During Aging

Mutations in genes affecting metabolism, mitochondrial functions, as well as endocrine and stress signaling cascades affect the lifespan of a variety of model organisms. The process of aging thus appears to be regulated by evolutionary conserved pathways that respond to sensory cues, stress, or caloric restriction. The development of aging-associated diseases is linked to a deregulation of these complex regulatory networks that ensure the intracellular surveillance of cellular homeostasis.
Projects within research area A aim at the molecular characterization of cellular mechanisms underlying the aging process itself and aging-associated diseases. Cellular stress responses activated by a dysfunction of mitochondria and ER stress are of central interest. Groups within this research area will examine the role of ROS damage and apoptosis as consequences of age-related mitochondrial DNA mutations and impaired mitochondrial morphogenesis during aging and will also focus on the elucidation of the functional interplay of cellular stress and metabolic signaling pathways. In parallel, neurodegenerative human disorders characterized by age-related symptoms will be studied. Using a large variety of experimental approaches and cutting-edge technologies including cellular and mouse models, research area A will provide an integrated view on cellular dysfunctions underlying aging as well as aging-associated diseases.

Coordinator:

Prof. Dr. Thomas Langer,
Institut für Genetik
 
email: Thomas.Langer(at)uni-koeln(dot)de