Our lab is interested in studying the defects of protein synthesis in the context of neurodegeneration, with a focus on Alzheimer’s disease (AD). We aim to understand how the dysregulation of protein synthesis could contribute to the synaptic dysfunction observed in AD. We focus on studying synaptic activity mediated protein synthesis and its defects in AD. To understand this, we study two major aspects – 1) the role of energy metabolism and 2) the role of calcium signaling, and how they are integrated to regulate synaptic/activity mediated protein synthesis. Exploring the link between energy metabolism and calcium homeostasis with synaptic protein synthesis is relevant in neurodegeneration as each of these aspects are individually shown to be affected. We use both human iPSC derived neurons and animal models of AD for our studies. In the case of iPSC derived neurons, we use iPSCs generated from familial AD patients, where the mutation has been corrected using CRISPR/Cas9 based gene editing. Similarly, we also use iPSCs from healthy individuals where the mutation has been knocked-in using CRISPR/Cas9 to generate the AD iPSC models. Apart from familial mutations, we also intend to make iPSCs from sporadic AD patients with known risk factors such as APOE4 to understand their contribution to AD pathology.