What Sets Our Science Apart

1 · Deep Brain Stimulation Acts Across Networks – and Takes Time

Long-term pallidal DBS does more than alter activity at the stimulation site. It reorganises synaptic patterns in the motor thalamus and cortex, normalises pathological activity in the cerebellum and reduces dystonia in the dtSZ model only after sustained continuous stimulation. This makes the delayed therapeutic effect mechanistically understandable as an expression of distributed network plasticity.

2 · Biomarkers and Models Make Neurostimulation More Precise

Biophysical large-scale network and volume-conductor models integrate anatomy, dynamics and stimulation. They identify frequency-dependent effects, promising target regions and measurable network states. Combined with modular stimulation platforms and high-density electrode arrays, they provide a foundation for predictive markers and adaptive, closed-loop DBS.

3 · Epileptogenesis Is a Disorder of Ion Channels and Immune Networks

Studies of KCa2/SK-, Kv7.2/7.3-, HCN- and GluN2B-dependent plasticity show how persistent channel changes shape synaptic excitability and disease progression. In parallel, antibody models demonstrate that autoimmune responses can directly alter neuronal circuits. These findings reveal targets for antiepileptogenic and immunomodulatory therapies.

4 · Stroke – a neurological dysfunction with complex pathomechanisms

According to the WHO, stroke is one of the leading causes of mortality and disability worldwide. In order to investigate the complex pathophysiological mechanisms in more detail, the institute utilizes various ex vivo and in vivo models to study ischemic and hemorrhagic stroke events. From these, neuroprotective mechanisms are derived and characterized, which aim to decisively improve future therapeutic options.

5 · Tumour Neurophysiology Connects Cancer Biology and Seizure Control

The Institute investigates gliomas as active components of neuronal networks. A glutamatergic biomarker panel distinguishes high-grade gliomas/astrocytomas from brain metastases; in the F98 model, cenobamate reduces epileptiform activity. High-density MEA recordings also offer a systematic route to the network phenotype of tumour-associated epilepsy.

6 · Electrical Fields Guide Cells, Tissue and Regeneration

Galvanotaxis and impedance studies show that electrical fields influence the migration of tumour cells and osteoblasts and can also be used to monitor tissue maturation. Experimental microbeam therapy further extends the classical Langendorff preparation into a model for functional testing of extreme spatially fractionated radiation.

Key Publications

1. Santana Kragelund et al. (2026). Investigating the Network-Wide Mechanisms of Pallidal Deep Brain Stimulation Using High-Density Microelectrode Arrays Journal of Visualized Experiments 232. A methodological reference for high-resolution analysis of distributed DBS effects.
2. Franz et al. (2025). Network-wide modulation of synaptic plasticity and spike patterns in motor circuits after pallidal deep brain stimulation in a dystonia model Neurobiology of Disease 214:107037. Demonstrates the reorganisation of thalamocortical synapses after long-term DBS.
3. Kotyra et al. (2025). Effects of longer-term pallidal stimulation on the severity of dystonia in a phenotypic animal model Experimental Neurology 396:115548. Confirms the delayed reduction in symptoms after ten days of continuous DBS.
4. Santana Kragelund et al. (2024). Network-wide effects of pallidal deep brain stimulation normalised abnormal cerebellar cortical activity in the dystonic animal model Neurobiology of Disease 205:106779. Establishes the cerebellum as part of the network-wide effects of pallidal DBS.
5. Spiliotis et al. (2024). Utilising activity patterns of a complex biophysical network model to optimise intra-striatal deep brain stimulation Scientific Reports 14:18919. Links network states with the computational optimisation of stimulation.
6. Müller et al. (2024). Persistent Kv7.2/7.3 downregulation in the rat pilocarpine model of mesial temporal lobe epilepsy Epilepsy Research 200:107296. Identifies persistent channel plasticity as a component of epileptogenesis.
7. Lange et al. (2024). A glutamatergic biomarker panel enables differentiating Grade 4 gliomas/astrocytomas from brain metastases Frontiers in Oncology 14:1335401. Translates glutamatergic tumour neurophysiology into a diagnostic biomarker strategy.
8. Forberger et al. (2025). Cenobamate reduces epileptiform activity in the ex vivo F98 rat glioma model Frontiers in Neuroscience 19:1629259. Opens a new pharmacological avenue for tumour-associated epilepsy.
9. Engel et al. (2023). Combining Electrostimulation with Impedance Sensing to Promote and Track Osteogenesis within a Titanium Implant Biomedicines 11:697. Demonstrates the integration of stimulation and sensing in regenerative implants.
10. Reichart et al. (2026). Reduced Cerebral Infarct Volume in Young UCP2−/− Mice and Preserved Synaptic Transmission by Genipin. Cells 2026, 15(14), 1299. Mild persistent oxidative stress help to diminish ischemia-reperfusion injury. Genipin act in a neuroprotective manner under hypoxia and reperfusion.

External Funding, Research Consortia and Scientific Alliances

DFG Collaborative Research Centre 1270 ELAINE · Project C03

Current · third funding period from 2026. C03 ‘Deep brain stimulation in dystonia models’ investigates long-term synaptic and cellular plasticity, cholinergic and dopaminergic modulation, and predictive biomarkers. Electrophysiology, high-density MEAs, immunohistochemistry and mathematical modelling are closely integrated with implant and stimulation technology. Project leads: Rüdiger Köhling and Franziska Richter Assêncio.

DFG Collaborative Research Centre 1270 ELAINE · Central Service Project S01

Current · third funding period from 2026. S01 ‘Improving metrology and instrumentation for electrostimulation experiments’ establishes a shared metrological foundation for the consortium. The project develops reusable methods for comprehensive characterisation of stimulation devices and electrodes across relevant frequencies, supports the use and encapsulation of in vitro and in vivo stimulation systems, and thereby strengthens standardisation, comparability and reproducibility. Project leads: Christian Haubelt and Denise Franz; her permanent appointment to the Oscar Langendorff Institute in 2024 also reflects the successful progression of ELAINE early-career researchers into independent leadership.

DFG-funded Foundational Research

Completed individual grants provide the mechanistic foundations of the Institute’s current profile:

• pathophysiology of primary paroxysmal dystonias in the genetic hamster model
• pathological regulation of SK potassium channels in epilepsy models
• presynaptic HCN channels, axonal transport and synaptic metaplasticity
• changes in neocortical excitability during glioma invasion

Transdisciplinary Collaboration

The Institute works closely with mathematics, theoretical electrical engineering, neurosurgery, neurology, urology, paediatric surgery, radiation oncology, tumour biology and materials science. This structure connects mechanistic physiology with modelling, implant development, human surgical tissue and clinically relevant endpoints.

Technology Platform

• Multiscale Electrophysiology: whole-cell patch clamp, field potentials, EEG/EMG and acute brain-slice preparations.
• High-density Network Recording: multi-electrode arrays, spatial activity maps and data-driven signal analysis.
• Neuromodulation: chronic DBS, modular preclinical stimulation systems, and frequency and target optimisation.
• Computational Neuroscience: biophysical network models, volume-conductor models and equation-free control.
• Translational Models: dystonia, epilepsy, stroke, glioma and autoimmune encephalitis; plus human resection tissue and patient-derived tumour cells.
• Electroactive Tissues: galvanotaxis, impedance measurement, electrical/mechanical stimulation and regenerative implants.
• Molecular Validation: immunohistochemistry, expression and biomarker analyses, and functional pharmacology.

Our Ambition: To understand physiological mechanisms with sufficient precision to generate measurable markers, testable models and better interventions – for diseases in which cells, networks and technical systems must be considered together.