Raja Bhatstacharyya, Ph.D.

Instructor of Neurology, Massachusetts General Hospital, Harvard Medical School


Dr. Raja Bhatstacharyya is a cell biologist and studies the cellular and molecular mechanisms of Alzheimer’s disease (AD) pathology. Dr. Bhattacharyya received his Ph.D. from Jadavpur University, Bose Institute, Calcutta, India. In his doctoral thesis, he studied fatty acylation of erythrocyte membrane protein 4.2 in chronic myeloid leukemia. In his post-doctoral research, Dr. Bhattacharyya uncovered aspects of fatty acylation, specifically palmitoylation, in regulating subcellular localization and functions of oncogenic proteins namely, Galpha12/13 and Rho/Rac GTPases. Later, Dr. Bhattacharyya extended his understanding of protein fatty acylation in AD research to first demonstrate that the beta-amyloid precursor protein APP is palmitoylated. He showed that palmitoylated APP (palAPP) and/or it’s dimerized form in lipid rafts are potential therapeutic targets for AD.

Dr. Bhattacharyya is an Instructor of Neurology in Dr. Rudolph Tanzi lab at Massachusetts General Hospital, Harvard Medical School. Dr. Bhattacharyya’s current research revealed that palAPP is stabilized and is prepared for cleavage by beta-secretase in special lipid rafts within the neuron known as mitochondria-associated ER membranes (MAMs). Most notably, Dr. Bhattacharyya’s research shows not only that the MAM is where palAPP is processed by beta-secretase to make Abeta, but that this happens exclusively in axons and neuronal processes where Abeta does most of its damage. His findings have significantly advanced the understanding of the cellular and molecular mechanisms underlying APP processing/trafficking and Abeta generation in axons and synapses. Dr. Bhattacharyya’s current research focuses on studying the effect of de-palmitoylating agents and cholesterol-modifying agents on Abeta generation from MAM-associated palAPP, specifically from axons and neuronal processes. Dr. Bhattacharyya’s research carries major implications for developing novel AD therapies based on targeting MAM-associated palAPP in neuronal processes and axons to ameliorate neuritic and synaptic Abeta pathology.