Belaidi Abdel A

Dr. Belaidi (Licentiate, Diplom, PhD) is a Senior Research Fellow at the Florey Institute of Neuroscience and Mental Health at the University of Melbourne, Australia. He is an expert in iron metabolism, ferroptosis, apolipoprotein E and apolipoprotein E receptors and their association with neurodegeneration with a special focus on mechanism of neurodegeneration in Alzheimer’s disease. He was awarded a PhD in Biochemistry at the University of Cologne in Germany in 2011 and continued his postdoctoral research in Germany in the field of molybdenum and sulphur amino acid metabolism and associated neuronal cell death. Dr. Belaidi’s research contributions included basic molybdenum biochemistry where he was able to decipher the last step of the biosynthesis of the molybdenum cofactor in humans where he characterized the function of gephyrin as the enzyme catalysing the last biosynthesis step of the cofactor and defined the function of each of its domains. Dr. Belaidi further refocused his interest in investigating the molecular basis of neuronal cell death associated with sulphite toxicity in a rare inborn error of metabolism termed molybdenum cofactor deficiency. His achievements in this area included the identification of excitotoxicity as a new mechanism of neuronal cell death in the disease. His research resulted in significant novel biochemical and clinical findings and has been translated to the development of the first successful therapy of human molybdenum cofactor deficiency type A. Dr. Belaidi was awarded an international research fellowship from the German Research foundation (DFG) and moved to Australia in 2015 where he undertook research in neuroscience with a special focus on mechanism of neuronal cell death associated with iron metabolism and was the recipient of a research fellowship and a research grant from the Alzheimer’s Association. Dr. Belaidi’s current research laboratory is specialized in investigating cell metabolism and cell death mechanisms implicated in neurodegeneration with particular interest in understanding the cross talk between cysteine, lipid and iron metabolism in determining neuronal susceptibility to cell death. His achievements in this area included the identification of apolipoprotein E as an inhibitor of cell death resulting from lipid peroxidation/ferroptosis in neurons, thus suggesting ferroptosis as a possible mechanism of neurodegeneration in Alzheimer’s disease.