Prof. Dr. Stefan Remy

Professor, Group Leader

German Center for Neurodegenerative Diseases (DZNE)
Sigmund-Freud-Str. 27 
53127 Bonn

+49 (0) 228 / 43302-684 (Secretary)

Group members

Name Phone
Nancy El Deiry, Assistant +49 (0)228 / 43302-684
Hiroshi Kaneko, Ph.D., Postdoc +49 (0)228 / 43302-671
Dr. Christina Müller, Postdoc +49 (0)228 / 43302-252
Dr. Rüdiger Geis, Postdoc +49 (0)228 / 43302-252
Dr. Yu-Chao Liu, Postdoc +49 (0)228 / 43302-257
Tatjana Beutel, cand. med. +49 (0)228 / 43302-257
Dipl. Math. Daniel Justus, Ph.D. Student +49 (0)228 / 43302-254
Dipl. Biol. Falko Fuhrmann, Ph.D. Student +49 (0)228 / 43302-254
Christian Hannes, M.Sc., Ph.D. Student (FZJ-DZNE Kooperation) +49 (0)228 / 43302-255
Dennis Dalügge, Ph.D. Student +49 (0)228 / 43302-253
Detlef Friedrichs, Technical Assistant +49 (0)228 / 43302-258
Yvonne Schleehuber, Technical Assistant +49 (0)228 / 43302-255
Irina Pavlova, Research Assistant +49 (0)228 / 43302-684
Meltem Eryilmaz, Student Assistant +49 (0)228 / 43302-255
Petra Mocellin, Student Assistant +49 (0)228 / 43302-257
Further group members (DFG-SFB 1089)
Dr. Liudmila Sosulina, Postdoc +49 (0)228 / 43302-253
Felix Ludwig M.Sc., Ph.D. Student +49 (0)228 / 43302-256
f.l.t.r.: Hiroshi Kaneko, Christian Hannes, Tatjana Beutel, Stefan Remy, Stefanie Bothe, Nancy El-Deiry, Meltem Eryilmaz, Liudmila Sosulina, Daniel Justus, Dennis Dalügge, Rüdiger Geis, Falko Fuhrmann, Felix Ludwig. Source: DZNE / Daniel Bayer
Group photo AG RemyClick on the magnifying glass for a large image.



Glutamatergic synaptic integration of locomotion speed via septo-entorhinal projections.

Justus D, Dalügge D, Bothe S, Fuhrmann F, Hannes C, Kaneko H, Friedrichs D, Sosulina L, Schwarz I, Elliott D, Schoch S, Bradke F, Schwarz MK, Remy S (2016) Nature Neuroscience (in press, scheduled for Jan 2017 issue with News and Views article).

Dysfunction of somatostatin positive interneurons associated with memory deficits in an Alzheimer's disease model.

Schmid LC, Mittag M, Poll S, Steffen J, Geis HR, Schwarz I, Schmidt B, Schwarz MK, Remy S, Fuhrmann M (2016) Neuron, 92(1):114-125.

Slowly building excitement.

Müller C., Remy S. (2016) Cell. 2016 Jun 16;165(7):1568-9. 

Reducing tau aggregates with anle138b delays disease progression in a mouse model of tauopathies.

Wagner J, Krauss S, Shi S, Ryazanov S, Steffen J, Miklitz C, Leonov A, Kleinknecht A, Göricke B, Weishaupt JH, Weckbecker D, Reiner AM, Zinth W, Levin J, Ehninger D, Remy S, Kretzschmar HA, Griesinger C, Giese A, Fuhrmann M. (2015) Acta Neuropathol. 2015 Nov;130(5):619-31.

Locomotion, theta oscillations and the speed-correlated firing of hippocampal neurons are mediated by a glutamatergic medial septal circuit.

Fuhrmann F, Justus D, Sosulina L, Kaneko H, Beutel T, Friedrichs D, Schoch S, Schwarz MK, Fuhrmann M, Remy S. Neuron. 2015 June 3; (IF: 15.9)


Dendritic structural degeneration is functionally linked to cellular hyperexcitability in a mouse model of Alzheimer’s Disease.

Šišková, Z., Justus, D., Kaneko, H., Friedrichs, D., Henneberg, N., Beutel, T., Pitsch, J., Schoch, S. , Becker, A., von der Kammer, H. and Remy, S. Neuron, 2014 Nov 13; (IF: 15.8)  

Inhibitory control of linear and supralinear dendritic excitation in CA1 pyramidal neurons.

Müller, C., Beck, H., Coulter, D., Remy, S. Neuron, 2012 (IF: 15.8)  

Dendritic integration in hippocampal granule cells.

Krüppel, R., Remy, S., Beck, H. Neuron, 2011 (IF: 15.8)  

A post-burst afterdepolarization is mediated by group I metabotropic glutamate receptor-dependent upregulation of Cav2.3 R-Type calcium channels in CA1 pyramidal neurons.

Park, J., Remy, S., Varela, J., Cooper D., Chung, S., Spruston N. PLoS Biology 2010 (IF: 11.7)   

Activity-dependent control of neuronal output by local and global dendritic spike attenuation.

Remy, S., Csicsvari, J., Beck, H. Neuron, 2009 (IF: 15.8)  

Dendritic spikes induce single-burst long-term potentiation.

Remy, S. and Spruston, N. Proceedings of the National Academy of Sciences PNAS 2007 (IF: 9.8)  

A novel mechanism underlying drug resistance in chronic epilepsy. Ann Neurol.

Remy S, Gabriel S, Urban BW, Dietrich D, Lehmann TN, Elger CE, Heinemann U, Beck H. Ann Neurol. 2003 Apr;53(4):469-79. (IF 11)

The complete list of publications is found here.

Curriculum Vitae

Areas of investigation/research focus

Dendritic integration of synaptic signals

Neurons form branched extensions, so called dendrites, which receive more than 95% of the input signals from other neurons. Signal processing depends on the properties and structure of these small-caliber dendrites. Changes in the way in which neurons process synaptic information form the cellular basis of learning and memory. Although the central role of dendrites in signal integration and synaptic plasticity has been recognized for decades, it has only become possible recently to study the properties of even the finest dendrites by modern two-photon and STED imaging techniques, electrophysiology and computational modeling (see Remy and Spruston 2007, Remy et al. 2009, Müller et al, 2012, Siskova et al, 2014).

Neural circuits underlying cognitive map formation

The hippocampal formation is an important part of our memory systems. It receives and processes external information about our environment and our position in space and uses this information to form and retrieve memories. We study the neural circuits that feed spatial information into our memory systems and try to understand the circuit operations that lead to memory formation and retrieval. The brain uses oscillations of hundreds of neurons, which can be visualized in an EEG or local field potential recordings, to coordinate the information flow during processing of spatial information. One important focus of our work is to understand how oscillations are generated and maintained during behavior (see Fuhrmann et al. 2015). We use two-photon GECI imaging, whole-cell patch-clamp recordings, single-unit tetrode recordings, LFP recordings and fiberoptometry during behavior to address these questions.

Dysfunction of neurons and neural circuits in neurodegenerative diseases

Alzheimer’s disease is the most common form of dementia, the risk for its development increases with each decade of adult life. It affects memory, thinking and behavior. At the present time no satisfying therapeutic approach exists to prevent the disease-related changes. A prerequisite for the development of such therapies is to gain a better understanding of the underlying molecular and structural disease-related changes of individual neuronal compartments such as single synapses on dendritic spines and dendrites. Even the smallest changes in the processing of synaptic signals can easily lead to a change in the output signal and thus cause a disturbance of the function of an entire neuronal network (see Siskova et al, 2014). On the network level, a balanced interplay of excitatory neurons and inhibitory interneurons is required to direct the information flow through our memory systems and to form and retrieve memories. Clinically relevant is a selective loss of specific types and of interneurons as well as neuromodulatory afferents in Alzheimer’s disease and other neurodegenerative diseases. We use computational, imaging and electrophysiological techniques to understand the structural and functional neural circuit remodeling that leads to cognitive dysfunction in neurodegenerative diseases (see Siskova et al, 2014).