Center for Dementia Research, Nathan Kline Institute
My research has attempted to delineate the molecular pathway that leads to Alzheimer’s disease pathology in different regions and in different cell types in the brain. This has guided my doctoral training at Medical College of Wisconsin where I investigated the effect of the protein Amyloid beta, the causative protein in Alzheimer’s disease, on the epoxygenase activity in cortex, hippocampus and cultured neuronal and glial cells. Epoxygenases metabolize arachidonic acid to eicosanoids, which are neuroprotective in nature. I further studied the effect of amyloid beta on mitochondrial dysfunction and the efficacy of the eicosanoids to block this effect in cultured hippocampal astrocytes. I have mastered a number of techniques including cell culture, measurements in mitochondrial bioenergetics and confocal microscopy. During my postdoctoral training at Weill Cornell Medical College (NY) I have studied the mitochondria-associated membranes (MAM) that tether the mitochondria to the endoplasmic reticulum and how oxidative stress can impair the structure and function of MAM, with an extensive training in 3D electron microscopy. I have continued my research in dissecting out the differences in the autophagy-lysosomal pathway in cultured neuronal and glial cells at The Nathan Kline Institute (NY).