Ising, Christina - CAP 29

Tauopathies including Alzheimer’s disease (AD) are neurodegenerative diseases characterized by intraneuronal accumulation of the tau protein as well as chronic neuroinflammation. Microglia, the innate immune cells of the brain, play a central role in these diseases and we previously identified activation of the NLRP3 inflammasome, a defense mechanism in the cells, as an important disease mediator in tauopathies. NLRP3 inflammasome activation can lead to pro-inflammatory cytokine secretion and pyroptotic cell death, but the underlying mechanisms and the contribution of microglial cell death to the diseases remain elusive. By using e.g. genetic mouse models, primary cultures and organotypic slice cultures, we now study how and which microglial cell death pathways influence tau pathology and cognitive deficits. 

Furthermore, as especially AD is clearly an age-associated disease, we are also interested in understanding the contribution of aged microglia to the disease. One hallmark of aging is senescence, a cellular state characterized by the resistance to apoptotic cell death, metabolic dysfunction and release of a senescence-associated secretory profile (SASP). To better understand this critical cellular phenotype, we investigate molecular mechanisms leading to microglial senescence and SASP formation and analyze effects of senescent microglia on neurons in the disease setting.

For more information about Dr. Ising’s work, please check this site Research Christina Ising or ResearchGate.

• CECAD Research Center
• CMMC Center for Molecular Medicine Cologne
• CRC 1403