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Biography

Walter E Müller is currently Professor Emeritus at the Department of Pharmacology, Biocenter Goethe University Frankfurt. He got his Ph.D. in Pharmacology at the University Mainz were he also worked as Assistant Professor until 1983, when he moved as Associate Professor to the Central Institute of Mental Health Mannheim,University Heidelberg. From 1997 to 2013 he was Full Professor of Pharmacology at the Biocenter University Frankfurt. He received several professional awards including the Fritz Külz Preis of the German Pharmacological society. The award in Psychopharmacology of the AGNP, he was awarded fellowship of the American College of Neuropsychopharmacology, and he is honorary member of the Austrian Society of Biological Psychiatry.He has published more than 500 papers. His h-index is 65, his, i10-index 28.

Abstract

Mitochondrial dysfunction has been shown over the last years as common final pathway for brain aging and Alzheimer disease. Might it also represent a promising treatment strategy? Ironically, the evidences available now go back to some rather old drugs.The best clinical data shows EGb761 (Ginkgo extract) which improves impaired mitochondrial function, reduces ROS and apoptosis, elevates ATP, improves respiratory chain function, and improves synaptic plasticity. Another old drug is piracetam, which is still used at in many countries worldwide to treat cognitive impairment in aging, brain injuries as well as dementia. Its acceptance of as an antidementia drug was hampered by the lack of a clear mechanism of action. Our’s and other’s recent data clearly show improvement of mitochondrial dysfunction due to brain aging and other situations of elevated oxidative stress including AD like pathology. Another example is dimebon, an old antiallergic drug developed in Russia. A phase II trial indicating substantial therapeutical improvementcould not be reproduced in a subsequent large-scale phase III trial.Dimebon also specifically improves mitochondrial function in many in vitro and in vivo experiments. While all three drugs seem to have different targets, for each mitochondrial improvement goes parallel with specific alterations of mitochondrial dynamics. None of the three is the magic bullet. However, they definitively are good enough to serve as proof of conceptfor improving mitochondrial function as a valid treatment strategy for AD and might serve as starting point for future drug development.

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