Neuroretreat 2025

Angelika Lampert

Director of the Institute of Neurophysiology, Speaker of the Scientific Center for Neuropathic pain Aachen SCN-AACHEN, Uniklinik RWTH Aachen University, Pauwelsstr. 30, 52074 Aachen, Germany.

Title of talk: Sodium channel pore region as a hot-spot for pain-linked mutations:
Patch clamp, MD simulation and First Principle approaches

Short Bio: Angelika Lampert, MD, is the director of the Institute of Neurophysiology at the RWTH Aachen University, Germany. She is the coordinator of the Sodium Channel Network Aachen (SCNAACHEN) and the Scientific Center for Neuropathic pain Aachen (SCNAACHEN) focusing on inherited neuropathic pain syndromes such as small fiber neuropathy linked to sodium channel mutations. Her research concentrates on the translation of laboratory findings to potential clinical treatment, either as a population therapy or personalized medicine. The Lampert lab focusses on 1) biophysics and structure-function relation of voltage-gated sodium channels and their mutations linked to pain, and 2) induced pluripotent stem cells (iPS-cells) and their differentiation into peripheral sensory neurons as a model for human neuropathies.
Dr. Lampert studied human medicine in Jena, Germany, and Strasbourg, France, and completed her MD thesis at the Max-Plank working group Molecular and Cellular Biophysics in Jena in 2003. Following postdoctoral training at Yale University in New Haven, CT, Angelika Lampert set up her lab in Erlangen, Germany, before moving to Aachen in 2013. Dr. Lampert is the recipient of awards and grants from the German Research Foundation (DFG), the Federal Ministry of Education and Research (BMBF) and the German Association of the Study of Pain (DGSS).

Highlights/Short abstract: Mutations in voltage-gated sodium channels are linked to inherited pain syndromes, such as chronic pain or chronic insensitivity to pain. Here I will present the case of a Chinese patient who has impaired pain sensation due to a missense mutation in the sodium channel Nav1.7 pore region. The substitution leads to a pore collapse, which helped us to identify a construct within the pore of all four domains to support the pore helices and selectivity filter.

More and more variants of unclear significance (VUS) are identified in Nav1.7 which poses a problem for clinicians as they need to communicate an interpretation of genetic findings to their patients. Using a first principle approach it is possible to decipher channel structure thermostability constraints and consequently predict pain-disease-associated hotspot locations. We show that with the model we can identify the pore region as a hotspot for pain-linked mutations.

Selected publications
1. Meents, J.E.*, E. Bressan*, S. Sontag*, A. Foerster*, P. Hautvast, C. Rösseler, M. Hampl, H. Schüler, R. Goetzke, T. K. Chi Le, I. P. Kleggetveit, K.Le Cann, C. Kerth, A. M. Rush, M. Rogers, Z. Kohl, M. Schmelz, W. Wagner, E. Jørum, B. Namer, B. Winner, M. Zenke, A. Lampert. “The role of Nav1.7 in human nociceptors: insights from human iPS cell-derived sensory neurons of erythromelalgia patients.” Pain. 2019 Jun;160(6):1327-1341. DOI: 10.1097/j.pain.0000000000001511

2. Markos N. Xenakis, Angelika Lampert. “Learning molecular traits of human pain disease via voltage-gated sodium channel structure renormalization”. BioRxiv 2025. DOI: https://doi.org/10.1101/2025.02.19.639033

3. Rühlmann, AH, J Körner, R Hausmann, N Bebrivenski, C Neuhof, S Detro-Dassen, P Hautvast, CA Benasolo, J Meents, JP Machtens, G Schmalzing, A Lampert. “Uncoupling sodium channel dimers rescues the phenotype of a pain-linked Nav1.7 mutation.” British Journal of Pharmacology, 2020 Jul 14. https://doi.org/10.1111/bph.15196

Philippe Lory

CNRS Research Director, Institut de Génomique Fonctionnelle (IGF), Université de Montpellier – CNRS – INSERM, France

Title of talk: de novo ion channel variants are an emerging cause of neurodevelopmental disorders

Short Bio: Trained in electrophysiology, I am currently leading the team ‘Ion Channels in Neuronal Excitability and Diseases’ at IGF - CNRS, Montpellier - France (~ 10 members including 4 tenured CNRS and INSERM scientists). My expertise covers ion channel physiology, regulation and channelopathies, especially for T-type Cav3 calcium channels. The calcium channelopathies that we study include forms of epilepsy, cerebellar disorders, neuropathic pain and neurodevelopmental deficits. We also investigate the sodium-leak channel NALCN and the functional consequences of disease-causing mutations in NALCN. My lab has developed a wide range of in vitro, in vivo (animal models) and in silico strategies to study the pathogenic mechanisms underlying these neuronal channelopathies.

Highlights/Short abstract: These recent years, our lab has contributed to document the many de novo variants of the T-type calcium channels (Cav3.1) and sodium leak channel (NALCN) leading to complex neurodevelopmental syndromes. This talk will overview some these important findings and perspectives of this work.

Selected publications
1. The characterization of new de novo CACNA1G variants affecting the intracellular gate of Cav3.1 channel broadens the spectrum of neurodevelopmental phenotypes in SCA42ND. Qebibo L*, Davakan A*, … Cantagrel V, Burglen L, Lory P. Genet Med. 2024 27(3):101337. doi: 10.1016/j.gim.2024.101337. PMID: 39674904

2. Monteil A, Guérineau NC, Gil-Nagel A, Parra-Diaz P, Lory P, Senatore A. New insights into the physiology and pathophysiology of the atypical sodium leak channel NALCN. Physiol Rev. 2024 104(1):399-472. PMID: 37615954.

3. Lory P, Nicole S, Monteil A. Neuronal Cav3 channelopathies: recent progress and perspectives. Pflugers Arch. 2020 472(7):831-844. PMID: 32638069.

Antonios Pantazis

Linköping University, Sweden

Title of talk: The hidden lives of presynaptic calcium channels

Short Bio: For the longest part of his life, Antonios has been excited about the proteins control cellular excitability: ion channels! He did his PhD in Cambridge on fruitfly ion channels, and evolved to studying mammalian ion channels for his first postdoc at University College London. After that, he spent 10 years at UCLA working on (you guessed it) ion channel biophysics. In 2018, he joined Linköping University as member of the Wallenberg Center for Molecular Medicine. His research focuses on how ion channels are regulated to perform critical signaling roles; and how mutations in ion channel genes affect their function and biosynthesis to cause serious neurological and cardiovascular disorders.

Highlights/Short abstract: CaV2-family presynaptic calcium channels convert an electrical signal (action potential) to a biochemical signal (calcium influx) that triggers neurotransmitter release. CaV2.1 control release in most brain synapses, while CaV2.2 are more specifically located in peripheral terminals, where they control the transmission of sensory information, like pain. Despite the importance of their function, they are “black boxes,” and their molecular mechanisms of activation and regulation remain unknown. We implemented the voltage-clamp flurometry approach on human CaV2 channels, to understand how they sense electrical signals, and how they are regulated by factors that affect synaptic output. Specifically, we probed the inhibition of CaV2.2 activation by G-proteins (a mechanism exploited by opioids) and CaV2.1 voltage-dependent inhibition (VDI), a form of molecular memory that contributes to lifelong memory formation and learning. We found that, in both channels, specialized voltage-sensor domains (VSDs) respond differently to electrical signals in terms of probability and rate of activation, giving rise to a spectacular multiplicity of channel conformations; and that VSDs are differentially regulated by G-proteins and prolonged sojourns of depolarization (VDI). By revealing the hidden conformational diversity underpinning the molecular physiology of human CaV2-channels, our work facilitates the development of novel analgesics and explains the emergence of fundamental aspects of plasticity and learning.

Selected publications
1. Nilsson M, Wang K, Mínguez-Viñas T, Angelini M, Berglund S, Olcese R, Pantazis A (2024) Voltage-dependent G-protein regulation of CaV2.2 (N-type) channels. Sci Adv. 10(37):eadp6665. https://doi.org/10.1126/sciadv.adp6665

2. Wang K, Nilsson M, Angelini M, Olcese R, Elinder F, Pantazis A (2025) A Rich Conformational Palette Underlies Human CaV2.1-Channel Availability. Nat Commun. [“ACCEPTED IN PRINCIPLE”—available now as pre-print at https://doi.org/10.1101/2024.09.27.615501]

George Tofaris

Professor of Neurology and Translational Neuroscience, University of Oxford, Great Britain

Title of talk:
Harnessing the interplay between alpha-synuclein and organelle homeostasis for biomarker development in Parkinson’s disease.

Short Bio:
George Tofaris is a Professor of Neurology & Translational Neuroscience at the University of Oxford and Honorary Consultant Neurologist at the John Radcliffe Hospital. He graduated from the MB/PhD programme of Cambridge University and trained in Internal Medicine and Neurology at London and Oxford University hospitals. He is currently an MRC Senior Clinical Fellow and previously held a Lefler Fellowship in Cell Biology at Harvard Medical School and a Wellcome Trust-Beit Prize Intermediate Fellowship at Oxford where he established his research group. The group employs a multifaceted approach including genetic screens, biochemical approaches and disease modelling in patient-derived induced pluripotent stem cells (iPSC) as well as the study of biosamples from clinical cohorts with a view to deciphering molecular mechanisms that could inform the development of therapeutics or biomarkers in Parkinson’s disease and related conditions.

Highlights/Short abstract:
Alpha-Synuclein accumulation and misfolding is central to the pathogenesis of Parkinson’s disease. We have delineated cellular pathways by which alpha-synuclein is targeted to the lysosome for degradation and mechanisms by which misfolded proteoforms impair this process. These insights in cellular models provided a rationale for the development of an extracellular vesicle-based biomarker to track the early (prodromal) phase of the Parkinson’s disease and to differentiate it from Parkinson’s-like conditions.

Selected publications
1. Yan S, Zhang W, Li X, Dutta S, Castle AR, Liu Y, Sahoo A, Lam CL, Gatford NJF, Hu MT, Li CZ, Jiang C, Shu B, Tofaris GK. Single extracellular vesicle detection assay identifies membrane-associated alpha-synuclein as an early-stage biomarker in Parkinson's disease. Cell Rep Med. 2025;6(3):101999. DOI: 10.1016/j.xcrm.2025.101999. PMID: 40056910

2. Yan S, Jiang C, Janzen A, Barber TR, Seger A, Sommerauer M, Davis JJ, Marek K, Hu MT, Oertel WH, Tofaris GK. Neuronally Derived Extracellular Vesicle alpha-Synuclein as a Serum Biomarker for Individuals at Risk of Developing Parkinson Disease. JAMA Neurol. 2024;81(1):59-68. DOI: 10.1001/jamaneurol.2023.4398. PMID: 38048087

3. Zenko D, Marsh J, Castle AR, Lewin R, Fischer R, Tofaris GK. Monitoring alpha-synuclein ubiquitination dynamics reveals key endosomal effectors mediating its trafficking and degradation. Science Adv. 2023;9(24):eadd8910. DOI: 10.1126/sciadv.add8910. PMID: 37315142

4. Jiang C, Hopfner F, Katsikoudi A, Hein R, Catli C, Evetts S, Huang Y, Wang H, Ryder JW, Kuhlenbaeumer G, Deuschl G, Padovani A, Berg D, Borroni B, Hu MT, Davis JJ, Tofaris GK. Serum neuronal exosomes predict and differentiate Parkinson's disease from atypical parkinsonism. J Neurol Neurosurg Psychiatry. 2020;91(7):720-729. DOI: 10.1136/jnnp-2019-322588. PMID: 32273329

Wilma D.J. van de Berg

PhD | Professor Cellular Neurodegeneration, in particular Parkinson’s disease | Cellular Neuroscientists and Neuroanatomist | Chair section Clinical Neuroanatomy and Biobanking (CNAB) | Director Normal Aging Brain Bank | Parkinson and Movement Disorders Centrum Amsterdam UMC | Dept. Anatomy and Neurosciences | Amsterdam UMC, Vrije University Amsterdam, Netherlands

Title of talk: Crowded organelles, damaged membranes and aggregated alpha-synuclein in the Parkinson’s disease human brain

Short Bio: Wilma D.J. Van de Berg is professor Cellular Neurodegeneration, neuroanatomist and chair of the section Clinical Neuroanatomy and Biobanking, dept. Anatomy and Neurosciences, Amsterdam UMC, Vrije University Amsterdam. She received her PhD in Cellular Neuroscience in 2003 at the University of Maastricht. Her research focuses on unravelling cellular disease mechanisms underpinning alpha-synuclein aggregation and selective neurodegeneration in Parkinson’s disease. She has ample experience with bio/brainbanking and high-end cellular imaging techniques. She is a member of the scientific advisory board of Alzheimer Nederland, scientific leader of the program ‘Neurodegeneration’, Amsterdam Neuroscience, and member of the steering committee of the Amsterdam Parkinson and Movement Disorders center. She is a founder and director of the ‘Normal Aging Brain Collection Amsterdam’ (NABCA) and leads a large multicenter observational cohort study ‘Profiling Parkinson’s’ (ProPARK) to improve personalized treatment in Parkinson’s. She is the president of the Dutch Parkinson Scientists association.

Highlights/Short abstract: Abnormal neuronal alpha-synuclein (aSyn) aggregation is a hallmark of synucleinopathies, such as Parkinson's disease (PD), and may stem from impaired protein clearance. aSyn aggregates are rich in membranous structures, including vesicles, lysosomes, and dysmorphic organelles, suggesting that the build-up of disrupted organelles contribute cellular dysfunction in PD. αSyn undergoes various post-translational modifications (PTMs) that critically affect its structure, aggregation propensity, and pathological role in synucleinopathies. This study aimed at investigating the abundance and localisation of αSyn proteoforms, including different PTMs, in human brain lysates, lysosomes and synaptic vesicles using quantitative immunoassays and multiplex immunofluorescence in combination with advanced confocal and STED microscopy. We show that only a small fraction of αSyn is phosphorylated at Serine 129 in control brain lysates and synapses, but both are markedly upregulated under pathological conditions. pSer129 synaptic enrichment is present in early stage PD and increased in remaining dopaminergic terminals. We demonstrate widespread accumulation of c-terminal truncated (CTT) αSyn in lysosomes in nigral dopaminergic neurons. Our findings reveal two co-existing pools of intracellular αSyn: 1) a synaptic and somatic pSer129 aSyn form; 2) a CTT lysosome- and mitochondrial associated form. We provide evidence of lysosomal involvement in cellular αSyn metabolism in the human PD brain and suggest that synaptic and lysosomal enrichment of αSyn might be an early event during the pathogenesis of PD. These findings highlight the potential role of promoting αSyn clearance by modulating lysosomal protease activity as a therapeutic strategy in early stage PD.

Selected publications
1. Moors TE, Maat CA, Niedieker D, Mona D, Petersen D, Timmermans-Huisman E, Kole J, El-Mashtoly SF, Spycher L, Zago W, Barbour R, Mundigl O, Kaluza K, Huber S, Hug MN, Kremer T, Ritter M, Dziadek S, Geurts JJG, Gerwert K, Britschgi M, van de Berg WDJ. The subcellular arrangement of alpha-synuclein proteoforms in the Parkinson's disease brain as revealed by multicolor STED microscopy. Acta Neuropathol. 2021 Sep;142(3):423-448. doi: 10.1007/s00401-021-02329-9. Epub 2021 Jun 11. PMID: 34115198; PMCID: PMC8357756.

2. Moors TE, Mona D, Luehe S, Duran-Pacheco G, Spycher L, Mundigl O, Kaluza K, Huber S, Hug MN, Kremer T, Ritter M, Dziadek S, Dernick G, van de Berg WDJ, Britschgi M. Multi-platform quantitation of alpha-synuclein human brain proteoforms suggests disease-specific biochemical profiles of synucleinopathies. Acta Neuropathol Commun. 2022 Jun 3;10(1):82. doi: 10.1186/s40478-022-01382-z. PMID: 35659116; PMCID: PMC9164351.

3. Preprint: doi: 10.1101/2024.07.25.605088

4. Moors TE, Morella ML, Bertran-Cobo C, Geut H, Udayar V, Timmermans-Huisman E, Ingrassia AMT, Brevé JJP, Bol JGJM, Bonifati V, Jagasia R, van de Berg WDJ. Altered TFEB subcellular localization in nigral neurons of subjects with incidental, sporadic and GBA-related Lewy body diseases. Acta Neuropathol. 2024 Apr 6;147(1):67. doi: 10.1007/s00401-024-02707-z. PMID: 38581586; PMCID: PMC10998821.

5. Preprint: doi: 10.21203/rs.3.rs-5325387/v1

Caroline Graff

Professor, clinical geneticist
Karolinska Institutet | Dept NVS | Center for Alzheimer Research |Division of Neurogeriatrics
Karolinska University Hospital-Solna | Clinical genetics and genomics | Unit for hereditary dementia
Karolinska University Hospital | Theme Inflammation and Aging

Title of talk: Translational genetic research in frontotemporal dementia and related neurodegenerative diseases.

Short Bio: Caroline Graff, MD, PhD, graduated as a medical doctor in 1992 and earned a PhD in clinical genetics in 1997 from Uppsala University. She conducted postdoctoral research in mitochondrial biology at Karolinska Institutet after which she started her research group in Translational genetics of neurodegenerative disease at Dept NVS, KI. Her work focuses on identifying genetic and other biomarkers for genetic frontotemporal dementia (GENFI-study) and genetic Alzheimer disease, aiming to improve genetic counseling and preventive strategies. Caroline is a clinical geneticist and leads the out-patient clinic for hereditary dementias at Dept of clinical genetics and genomics, Karolinska University Hospital, the Swedish FTD Initiative (frontallobsdemens.se), the brain bank at KI and the FTD-ALS research network at KI.

Highlights/Short abstract: Neurodegenerative diseases (NDDs) encompass a diverse array of disorders, such as dementias, that impact both the central and peripheral nervous systems, typically manifesting in adulthood. Diagnosing these conditions is often difficult due to the similarity in symptoms, pathology, and biomarker profiles. A definitive diagnosis usually requires postmortem neuropathological examination or molecular genetic testing. Despite extensive research efforts, there are currently no treatments available that can modify or cure these diseases. The purpose of our research studies is to identify and stage the temporal order of change in biomarkers that can be associated with autosomal dominant Frontotemporal dementia (FTD) ± ALS and autosomal dominant Alzheimer disease (ADAD). Biomarker discovery here means both liquid biomarkers measured in CSF and plasma, and biomarkers measured by imaging, EEG and cognitive testing as well as genetic variants associated with disease phenotypes.
To achieve this, we perform longitudinal clinical assessments and tissue sampling in families with known mutations and study the effects of the mutations in patient-derived samples and their effect on cognition, MRI and EEG. By assessing family members at presymptomatic stages, we can identify biomarker changes that occur before the disease becomes symptomatic and determine the sequence of these changes over time.
Our genetic approach provides individualized, mutation-specific information which gives us possibilities for personalized medicine. Studies on presymptomatic mutation carriers also provide a unique opportunity to study the otherwise hidden, preclinical stages of disease including possible early neurodevelopmental effects in young adults and youth. Guided by our results, we can determine the optimal time for treatment and treatment targets, which may change during the disease course. Our international collaborations guarantee power and a global impact of our results.
Our GENFI research studies and global collaborations have contributed to the planning and execution of several clinical treatment trials for genetic FTD caused by GRN and C9orf72 mutations and our site in Stockholm is included in two trials (NCT04931862 and NCT04374136).

Selected publications
1. Ehn E, Eisfeldt J, Laffita-Mesa JM, Thonberg H, Schoumans J, Portaankorva AM, Viitanen M, Lindstrand A, Nennesmo I, Graff C. A de novo, mosaic and complex chromosome 21 rearrangement causes APP triplication and familial autosomal dominant early onset Alzheimer disease. Scientific Reports 2025;15:2912. DOI: 10.1038/s41598-025-86645-0.

2. Johansson C, Thordardottir S, Laffita-Mesa J, Pannee J, Rodriguez-Vieitez E, Zetterberg H, Blennow K, Graff C. Gene-variant specific effects of plasma amyloid-β levels in Swedish autosomal dominant Alzheimer disease. Alzheimer's Research & Therapy 2024;16:207. DOI: 10.1186/s13195-024-01574-w.

3. Ullgren A, Öijerstedt L, Olofsson J, Bergström S, Remnestål J, van Swieten JC, Jiskoot LC, Seelaar H, Borroni B, Sanchez-Valle R, Moreno F, Laforce R, Synofzik M, Galimberti D, Rowe JB, Masellis M, Tartaglia MC, Finger E, Vandenberghe R, de Mendonça A, Tirabosch P, Santana I, Ducharme S, Butler CR, Gerhard A, Otto M, Bouzigues A, Russell L, Swift IJ, Sogorb-Esteve A, Heller C, Rohrer JD, Månberg A, Nilsson P, Graff C, Genetic Frontotemporal Dementia Initiative (GENFI). Altered plasma protein profiles in genetic FTD - a GENFI study. Molecular Neurodegeneration 2023;18:85. DOI: 10.1186/s13024-023-00677-6.

4. Johansson C, Thordardottir S, Laffita-Mesa J, Rodriguez-Vieitez E, Zetterberg H, Blennow K, Graff C. Plasma biomarker profiles in autosomal dominant Alzheimer's disease. BRAIN 2023;146:1132-1140. DOI: 10.1093/brain/awac399

Helen Farrants

Janelia Research Campus, Howard Hughes Medical Institute (HHMI), Ashburn, VA, USA

Title of talk: Engineering proteins to see more - multiplexed imaging of cellular activities in the brain

Short Bio: Helen Farrants is currently a Postdoctoral Associate working with Eric Schreiter at the Janelia Research Campus to engineer molecular tools to visualize physiology and neuroscience at scales that range from cells to living animals.

Helen earned a Ph.D. at the Swiss Federal Institute of Technology in Lausanne (EPFL), Switzerland, and the Max Planck Institute (MPI) for Medical Research, Germany, studying how to control proteins inside living cells. She is also a guest lecturer at Northern Virginia Community College and Howard University.

Highlights/Short abstract:
Fluorescence imaging of cellular activities with high spatial and temporal resolution has been vital for understanding the underlying molecular mechanisms of behavior. Genetically encoded indicators engineered from fluorescent proteins, such as GCaMP, have been especially useful, but they have a fixed emission color, and we currently lack bright indicators in the near infrared. The shortcomings of traditional indicators make the understanding of more complex cellular events in neuroscience by multiplexed imaging difficult. In this talk, I will present chemigenetic indicators, engineered from genetically encoded proteins and bright small-molecule dye-ligands, allowing flexibility in the emission color. This flexibility has allowed us to perform multiplexed imaging in the green to the near infrared of metabolic and cellular activities during reduced resources and in seizure-like states. Engineering new fluorescent indicators will further help illuminate cellular complexities of neuroscience.

Selected publications
1. Farrants H. et al, 2024, “A modular chemigenetic calcium indicator for multiplexed in vivo functional imaging” https://doi.org/10.1038/s41592-024-02411-6
2. Farrants H. and Tebo A. G., 2022, “Fluorescent chemigenetic actuators and indicators for use in living animals” https://doi.org/10.1016/j.coph.2021.12.007
3. Moret A., Farrants H.,… 2025, “An expanded palette of bright and photostable organellar Ca2+ sensors” https://doi.org/10.1101/2025.01.10.632364
4. Deo C.,[…] Farrants H., […], 2021, The HaloTag as a general scaffold for far-red tunable chemigenetic indicators https://doi.org/10.1038/s41589-021-00775-w

Xenofon Strakosas

Laboratory of Organic Electronics (LOE), Department of Science and Technology (ITN), Linkoping University, Sweden

Title of talk: in vivo fabricated organic based electrodes for targeted treatment and non-invasive brain machine interfaces

Short Bio: Xenofon Strakosas is an Assistant Professor at Linköping University, where he is affiliated with the Laboratory of Organic Electronics (LOE). His research primarily focuses on organic bioelectronics, exploring the transduction between electronic signals and ionic/molecular signals in electroactive surfaces, iontronic chemical delivery and circuitry, biosensors, next-generation medical therapies.

Highlights/Short abstract: Organic mixed ion and electron conductors (OMIECs) are integral to bioelectronic interfaces and organic devices. Conventional OMIEC synthesis methods—liquid-phase oxidative polymerization, vapor-phase oxidative polymerization, and electrochemical polymerization—offer distinct advantages but also face significant limitations, especially when interfacing with biological tissues. We present two innovative strategies for the in-situ development of OMIECs within living tissue. Drawing inspiration from natural processes, we utilize thiophene-based monomers and enzymatic reactions to form conductive polymer gels directly within the nervous system. Additionally, we have designed an organic monomer that responds to visible light, enabling the formation of self-doped conducting polymers. Both approaches have been successfully applied to create organic conductors in vivo and are used as active materials in organic electrochemical transistors. These novel methodologies overcome the constraints of traditional synthesis techniques, opening new avenues for designing soft, biocompatible, and high-performance electronic interfaces.

Selected publications
1. Strakosas Xenofon*†., Biesmans Hanne†., Abrahamsson Tobias., Hellman Karin., Ejneby Malin Silverå., Donahue Mary.., Ekström Peter., Ek Fredrik., Savvakis Marios., Hjort Martin., Bliman David., Linares Mathieu., Lindholm Caroline., Stavrinidou Eleni., Jennifer Y. Gerasimov., Simon. T. Daniel. Olsson. Roger., and Berggren Magnus*., Metabolite-induced in vivo fabrication of substrate-free organic bioelectronics, Science 379, 6634, 795-802, (2023). DOI: 10.1126/science.adc9998

2. Fredrik Ek, Tobias Abrahamsson, Marios Savvakis, Stefan Bormann, Abdelrazek H. Mousa, Muhammad Anwar Shameem, Karin Hellman, Amit Singh Yadav, Lazaro Hiram Betancourt, Peter Ekström, Jennifer Y. Gerasimov, Daniel T. Simon, György Marko-Varga, Martin Hjort, Magnus Berggren, Xenofon Strakosas and Roger Olsson*, In Vivo Photopolymerization: Achieving Detailed Conducting Patterns for Bioelectronics, Advanced Science 2408628. (2024) DOI: 10.1002/advs.202408628

3. Hanne Biesmans†, Alex Bersellini Farinotti†, Tobias Abrahamsson, Katriann Arja, Caroline Lindholm, Xenofon Strakosas, Jennifer Y. Gerasimov, Daniel T. Simon, Camilla I. Svensson*, Chiara Musumeci*, Magnus Berggren,. From synthetic vesicles to living cells: Anchoring conducting polymers to cell membrane. Science Advances, 10, 50. (2024). DOI: 10.1126/sciadv.adr2882

Christian Gossler

Institute for Auditory Neuroscience (IAN), University Medical Center Göttingen, Germany

Title of talk: Development of optical cochlear implants based on waveguide probes

Short Bio: Dr. Goßler's academic journey began with a diploma in Physics from the University of Regensburg in 2010. He then pursued his PhD at the Fraunhofer Institute for Applied Solid State Physics and the Department of Microsystems Engineering at the University of Freiburg, earning his doctorate in 2016.
Following his doctoral studies, Dr. Goßler held postdoctoral positions at the University of Freiburg and the Technical University of Chemnitz. In 2019, he co-founded OptoGenTech GmbH, a company dedicated to developing optogenetic multichannel stimulators for biomedical research and clinical applications.
Since 2022, Dr. Goßler has been leading the Optics Modules Group at the University Medical Center Göttingen. His research focuses on developing optical modules for cochlear implants, utilizing multi-channel waveguide technology to transmit light with high spatial resolution to the inner ear. This innovative approach aims to improve hearing restoration by providing more precise stimulation of auditory neurons.

Highlights/Short abstract: Cochlear implants (CIs) are the most successful neuroprostheses, enabling speech comprehension in the majority of the million otherwise deaf patients. However, there remains a major unmet medical need for improving the quality of hearing with CIs. Optogenetic stimulation of the cochlea has been suggested as an alternative approach for hearing restoration. To realize this technology, optical cochlear implants (oCIs) have been developed, which optogenetically stimulate spiral ganglion neurons (SGNs) via an optical pulse generated outside the cochlea. These pulses are guided to the SGNs inside the cochlea via flexible polymer-based waveguide probes. To couple these waveguide probes, an optical multichannel coupling system has been developed, which enables the coupling of multiple individual optical channels. The system is based on a microlens array, which allows for uniform coupling over all channels as well as specific coupling for each channel individually with minimal crosstalk. The microlens array is fabricated on a fused silica chip and contains an orthogonal grid of microlenses, of which a row is used for coupling. This development promises to improve the quality of hearing with CIs and is a crucial step towards the clinical translation of optogenetic cochlear implants, which have the potential to restore hearing in individuals with severe to profound hearing loss.

Selected publications
1. Huet, A., Mager, T., Gossler, C., & Moser, T. (2024). Toward optogenetic hearing restoration. Annual Review of Neuroscience. https://doi.org/10.1146/annurev-neuro-070623-103247

2. Kunze, K., Gossler, C., Peters, V., Keppeler, D., Moser, T., & U. T. Schwarz. (2024). Microlens arrays for multichannel laser-to-waveguide coupling. Applied Optics, 63(22), 5876–5885. https://doi.org/10.1364/AO.522367

3. Helke, C., Reinhardt, M., Arnold, M., Schwenzer, F., Haase, M., Wachs, M., Gossler, C., Götz, J., Keppeler, D., Wolf, B. J., Schaeper, J. J., Salditt, T., Moser, T., Schwarz, U. T., & Reuter, D. (2023). On the fabrication and characterization of polymer-based waveguide probes for use in future optical cochlear implants. Materials, 16(1), 106. https://doi.org/10.3390/ma16010106

Adam Williamsson

Center for Social and Affective Neuroscience (CSAN), Dept. of Biomedical and Clinical Sciences, Linköping University

Title of talk: Non-invasive Temporal Interference Stimulation of the Hippocampus Suppresses Epileptic Biomarkers in Patients with Epilepsy: Biophysical Differences between Kilohertz and Amplitude Modulated Stimulation

Short Bio: Adam Williamson is a Professor of Neurophysiology at Linköping University, Sweden, and a Research Team Leader at St. Anne’s University Hospital in Brno, Czech Republic. He received a bachelors and masters in electrical engineering from Texas Tech University, USA, and obtained his doctorate at the Technical University of Ilmenau, Germany. Previously, he served as research scientist at the Institute of Neuroscience (INS), a part of Inserm at Aix-Marseille University (AMU) in France. He is a recipient of 5 European Research Council (ERC) grants. His research focuses on in vivo applications of new electronic devices and methods of brain stimulation.

Highlights/Short abstract: Medication-refractory focal epilepsy creates a significant challenge, with approximately 30% of patients ineligible for surgery due to the involvement of eloquent cortex in the epileptogenic network. For such patients with limited surgical options, electrical neuromodulation represents a promising alternative therapy. In this study, we investigate the potential of non-invasive temporal interference (TI) electrical stimulation to reduce epileptic biomarkers in patients with epilepsy by comparing intracerebral recordings obtained before, during, and after TI stimulation, to recordings during low and high kHz frequency (HF) sham stimulation.
Thirteen patients with symptoms of mesiotemporal epilepsy (MTLE) and implanted with stereoelectroencephalography (sEEG) depth electrodes received TI stimulation with an amplitude modulation (AM) frequency of 130Hz (Δf), where the AM was delivered with lower frequency kHz carriers (1kHz + 1.13kHz), or higher frequency carriers (9kHz + 9.13kHz), targeting the hippocampus – a common epileptic focus and consequently stimulation target in MTLE. Our results show that TI stimulation yields a statistically significant decrease in interictal epileptiform discharges (IEDs) and pathological high-frequency oscillations (HFOs) – specifically fast-ripples (FR) –, where the suppression is apparent in the hippocampal focus and propagation from the focus is reduced brain-wide. HF sham stimulation at 1kHz frequency also impacted the IED rate in the cortex, but without reaching the hippocampal focus. The HF sham effect diminished with increasing frequencies (2, 5, and 9kHz, respectively), specifically as a function of depth into the cortex. This depth dependence was not observed with the TI, independent of the employed carrier frequency (low or high kHz). Furthermore, a strong carry-over effect, i.e., suppression of epileptic biomarkers for a period of time after the end of stimulation, was observed for TI but not for kHz. Our findings underscore the possible application of TI in epilepsy, as an additional non-invasive brain stimulation tool, potentially offering opportunities to assess brain region response to electrical neuromodulation before committing to a deep brain stimulation (DBS) or responsive neurostimulation (RNS) implants. Our results further demonstrate distinct biophysical differences between kHz and focal AM stimulation.

Selected publications
1. Missey et al., “Non-invasive Temporal Interference Stimulation of the Hippocampus Suppresses Epileptic Biomarkers in Patients with Epilepsy: Biophysical Differences between Kilohertz and Amplitude Modulated Stimulation”, medarchive, Clinical Trial Number NCT06716866 https://www.medrxiv.org/content/10.1101/2024.12.05.24303799v1

2. Lamos et al., “Noninvasive Temporal Interference Stimulation of the Subthalamic Nucleus in Parkinson's Disease Reduces Beta Activity”, Movement Disorders (2025) https://movementdisorders.onlinelibrary.wiley.com/doi/10.1002/mds.30134

3. Violante et al., “Non-invasive temporal interference electrical stimulation of the human hippocampus”, Nature Neuroscience (2023) https://www.nature.com/articles/s41593-023-01456-8