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Tibor Kristian, PhD

Research activity in our lab can be divided into two major projects: 1) The role of cell-type specific mitochondrial dynamics in acute brain injury; 2) Impact of changes in NAD+ metabolism on the cell death mechanism in neurodegenerative disease. Our recent studies, which utilize transgenic animals expressing neuronal and astrocytic mitochondria-targeted fluorescent marker in the brain, shows a differential response of cell-type specific mitochondria to stress conditions. We first reported that the mitochondria in neurons destined to die are not able to re-fuse following ischemia-induced fragmentation (Owens et al. 2015).

It is well established that massive degradation of cellular NAD+ can significantly compromise cell survival. Recently, we reported that administration of nicotinamide mononucleotide (NMN), a precursor for NAD+ synthesis, inhibits NAD+ degradation and leads to dramatic protection against ischemic brain injury (Park et al. 2016). We are now characterizing the mechanisms of NMN neuroprotection by determining the post-translational modifications of proteins controlling mitochondrial dynamics.