Thomas Moeller

moeller@u.washington.edu
Research Associate Professor, Department of Neurology

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Microglial cells are the resident immune cells of the central nervous system. Upon brain damage these cells get rapidly activated and transform from a resting state into activated microglia. This transformation includes significant immunological, metabolic and morphological changes which finally result in a phagocytic macrophage. Even though the phenomenon of microglia activation has been known for over 60 years the first steps in the activation cascade still remain unclear. It is widely believed that substances released from damaged cells within the brain trigger this process and consequently lead to the long-term changes of microglial gene expression and reorganization of the cell phenotype.

Recent publications enhanced our understanding of the mechanisms of [Ca2+]i homeostasis and signaling in microglial cells. It has been demonstrated that cultured microglial cells express several receptors linked to cytoplasmic Ca2+ elevations, including receptors for ATP, complement factors C5a and C3a, endothelins, noradrenaline and thrombin. All these receptors have been implicated to play an important role in pathophysiologies like stroke, Alzheimer's disease or multiple sclerosis.

In my research I am interested in the physiology of microglial cells and their involvement in pathophysiological mechanisms in the CNS. This includes the search for new receptors and their involvement in brain pathologies, the signal transduction pathways, which convey the receptor activation and the cellular responses to these stimuli. The methods used are cell physiological (i.e. fluorescent imaging techniques (Ca2+, Na+, H+), motility assays), biochemical (ELISA, proliferation assays, Western blot, immunostaining) and molecular (RNA-extraction, RT-PCR, gene arrays).