Role of ER-mitochondria contact sites in pathogenesis of Alzheimer's disease

• Applicant: Dr. Bernadette Schreiner
• Subject Area: Molecular and Cellular Neurology and Neuropathology ; Molecular Biology and Physiology of Neurons and Glial Cells
• Term: from 2013 to 2015
• Project identifier: Deutsche Forschungsgemeinschaft (DFG) - Project number 246276692

Alzheimers disease is the most common form of dementia affecting millions of people worldwide. Alzheimers disease is characterized by the progressive loss of neurons leading to a stepwise cognitive decline, and eventually death, of the patient. Today, there are no drugs available that can stop or delay the ongoing neurodegenerative process. The most prominent hallmarks in the Alzheimers disease brain are the intra- and extracellular accumulation of aggregated proteins. However, it could not be proved that these aggregates cause the synapse dysfunction and loss of neurons leading to the cognitive decline. Only recently, specialized lipid raft-like structures, the ER-mitochondria contact sites have moved in the focus of researchers in the Alzheimer field. They have been shown to be involved in the regulation of calcium metabolism, which is strongly altered in Alzheimers disease brain. This study proposes to extensively analyze the components of the ER-Mitochondria contact sites, which are involved in calcium signaling, in order to determine their role in the pathogenesis and their feasibility as targets for a new generation of drugs.

• DFG Programme: Research Fellowships
• International Connection: Sweden
• Host: Professorin Dr. Maria Ankarcrona