Alexander Dityatev

Alexander Dityatev, PhD

Molecular Neuroplasticity

DZNE – German Center for Neurodegenerative Diseases


Phone: 49 228 433020

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Since 2012 Alexander Dityatev is the head of the Molecular Neuroplasticity research group at DZNE and a full professor at the University of Magdeburg. His group is studying the role of extracellular matrix (ECM) molecules in major brain diseases and develops new strategies to image and target the ECM. The group combines expertise in vitro and in vivo electrophysiology, in vivo two-photon imaging and molecular biology.

Alexander Dityatev graduated in Mathematics at the Leningrad State University in 1985. In 1991 he accomplished his PhD in Biology with a thesis on quantal analysis of glutamate release at the Sechenov Institute of Evolutionary Physiology and Biochemistry in Leningrad. In 1992-1996, he worked with Peter Clamann as a postdoctoral fellow at the Department of Physiology, University of Bern, where he studied relationships between the structure and function of synaptic connections in the spinal cord. He then worked with Melitta Schachner as a group leader at the Center for Molecular Neurobiology Hamburg. There Dr. Dityatev with his colleagues uncovered synaptic functions of several cell adhesion and extracellular matrix molecules, such as tenascins, chondroitin sulfate proteoglycans, NCAM, L1, CHL1, and their associated glycans, including HNK-1 and PSA. Many of these functions turned out to involve interplay between recognition molecules and ligand- or voltage gated ion channels, resulting in regulation of perisomatic GABAergic inhibition, hippocampal long-term potentiation/depression and contextual memory. In 2004-2007, Alexander Dityatev was a German Research Foundation Fellow at the University Medical Center Hamburg-Eppendorf. In 2007-2012, being a Senior Researcher at the Italian Institute of Technology (IIT), Dr. Dityatev published several mechanistic studies uncovering how synaptic plasticity and learning are regulated by polysialylated form of NCAM and hyaluronic acid through regulation of extrasynaptic GluN2B receptors and L-type Ca2+ channels.