Raymond Chuen-Chung Chang
Department of Anatomy, LKS Faculty of Medicine
The University of Hong Kong, China
Dr. Chang received his BSc training in Biochemistry in Hong Kong. Then he furthered my MPhil training in neurochemistry and neuroanatomy at the same university. He received a research scholarship by German Academic Exchange Service DAAD to pursue his doctoral training in neurophysiology and clinical neuroscience at the University of Munich, Munich, Germany. Afterwards, he continued his postdoctoral training in neuropharmacology and molecular neuroscience at NIEHS/NIH, USA. During that time, he received the Visiting Research Fellowship Award and the NIH Fellow Award for Research Excellence by the National Institutes of Health. He has published over 70 peerreviewed publications and book chapters in neurodegeneration, neuroimmunology and drug discovery in these areas. Dr. Chang is now the Scientific Advisory Board member in International Alzheimer’s / Parkinson’s diseases Symposium, editorial board member in many different journals. Dr. Chang is also the Founder and Secretary of HKU Alzheimer’s Disease Research Network.
Dr. Chang’s research interest is to investigate molecular mechanisms of neurodegeneration in Alzheimer’s disease, Parkinson’s disease, ALS, glaucoma and aging-related macular degeneration (AMD) so that pharmacological targets can be found. Dr. Chang has studied neuronal apoptosis. He and his colleagues are among the first to discover a stress kinase, called double-stranded RNA-dependent protein kinase (PKR), plays important role in beta-amyloid peptide-induced neuronal apoptosis. He then investigated the damage of intracellular organelles, endoplasmic reticulum (ER) and mitochondria, in neurodegeneration and how their damage triggers autophagy (self-eating process) to struggle for survival. His group discovered the aggregation of the ER stimulate the nucleation step of autophagy. His group is now focusing how risk factors, depression and systemic inflammation, affect the synapses. He is also investigating how ER-stress responses and phosphorylation of tau protein propagate neurodegeneration. All these studies can be extended to neurodegeneration in glaucoma and AMD.