Dr. Vasileia Ismini Alexaki
B6: Technische Universität Dresden, Germany
Faculty of Medicine, Department of Clinical Pathobiochemistry
Junior group leader
Microglial cells are the resident immune cells of the Central Nervous System. Under normal conditions they exist in a quiescent state maintaining homeostasis. Upon trigger by an insult, such as a pathogen or an injury, they get activated acquiring anti-microbial and phagocytic features. Normally, the acute phase of inflammation is followed by a resolution phase, during which microglia return to a quiescent state. If resolution is perturbed, chronic inflammation may lead to neurodegeneration. Chronic neuroinflammation is a feature of many neurodegenerative diseases, such as Alzheimer’s disease and multiple sclerosis.
We are exploring regulatory mechanisms of microglia-mediated neuroinflammation. The neurotrophin Neural Growth Factor (NGF) was found to negatively regulate microglial activation and reduce its glycolytic activity. In accordance, the neurosteroid dehydroepiandrosterone (DHEA) exerts similar anti-inflammatory effects through activation of the NGF receptor, TrkA. Application of small lipophilic ligands of TrkA, like DHEA, which can penetrate the BBB and selectively activate TrkA signaling in microglia, could be envisioned as a means to control innate immune responses in the CNS.
Role in EuroNeurotrophin
Main Supervisor ESR 8
Leader of WP4