Kerschensteiner Lab | Neuroimmunology Munich

In multiple sclerosis immune cells infiltrate brain and spinal cord where they damage neurons and glial cells. This structural damage to the nervous system is responsible for the irreversible functional deficits that patients acquire over time. In our work we try to understand how immune cells damage the nervous, how reciprocal interactions between immune and nervous system control the formation and resolution of such inflammtory reactions and how we can best leverage this knowledge to design therapeutic approaches that prevent or limit tissue damage in multiple sclerosis.

We want to understand how immune cells damage axons in neuroinflammatory lesions. We have identified Focal Axonal Degeneration as a cellular mechanism of immune-mediated axon degeneration in both experimental and human neuroinflammatory lesions. As the early stages of this process are reversible we are now trying to unravel which cellular processes and molecular signals drive axons towards fragmentation or allow them to recover.

Project-related publications

Tai YH, Engels D, Locatelli G, Emmanouilidis I, Fecher C, Theodorou D, Müller SA, Licht-Mayer S, Kreutzfeldt M, Wagner I, de Mello NP, Gkotzamani SN, Trovò L, Kendirli A, Aljović A, Breckwoldt MO, Naumann R, Bareyre FM, Perocchi F, Mahad D, Merkler D, Lichtenthaler SF, Kerschensteiner M, Misgeld T. (2023). Targeting the TCA cycle can ameliorate widespread axonal energy deficiency in neuroinflammatory lesions. Nature metabolism, 5(8), 1364–1381.

Witte ME, Schumacher AM, Mahler CF, Bewersdorf JP, Lehmitz J, Scheiter A, Sánchez P, Williams PR, Griesbeck O, Naumann R, Misgeld T, Kerschensteiner M. Calcium Influx through Plasma-Membrane Nanoruptures Drives Axon Degeneration in a Model of Multiple Sclerosis. Neuron 2019 Feb 20;101(4):615-624

Sorbara CD, Wagner NE, Ladwig A, Nikić I, Merkler D, Kleele T, Marinković P, Naumann R, Godinho L, Bareyre FM, Bishop D, Misgeld T, Kerschensteiner M. Pervasive axonal transport deficits in multiple sclerosis models. Neuron 2014 Dec 17;84(6):1183-90.

Nikić I, Merkler D, Sorbara C, Brinkoetter M, Kreutzfeldt M, Bareyre FM, Brück W, Bishop D, Misgeld T, Kerschensteiner M. A reversible form of axon damage in experimental autoimmune encephalomyelitis and multiple sclerosis. Nat Med. 2011 Apr;17(4):495-9.

We are interested in resolving where and how oligodendrocytes are attacked by immune cells. Our work shows that damage often follows an outside-in pattern resulting in amputated oligodendrocytes. We now want to understand the fate of these cells during the formation and recovery of demyelinating lesions.

Project-related publications

Mezydlo A, Treiber N, Ullrich Gavilanes EM, Eichenseer K, Ancău M, Wens A, Ares Carral C, Schifferer M, Snaidero N, Misgeld T, Kerschensteiner M. Remyelination by surviving oligodendrocytes is inefficient in the inflamed mammalian cortex. Neuron. 2023 Apr 13:S0896-6273(23)00227-1.

Snaidero N, Schifferer M, Mezydlo A, Zalc B, Kerschensteiner M, Misgeld T. Myelin replacement triggered by single-cell demyelination in mouse cortex. Nat Commun. 2020 Sep 29;11(1):4901.

Romanelli E, Merkler D, Mezydlo A, Weil MT, Weber MS, Nikić I, Potz S, Meinl E, Matznick FE, Kreutzfeldt M, Ghanem A, Conzelmann KK, Metz I, Brück W, Routh M, Simons M, Bishop D, Misgeld T, Kerschensteiner M. Myelinosome formation represents an early stage of oligodendrocyte damage in multiple sclerosis and its animal model. Nat Commun. 2016 Nov 16;7:13275.

Mononuclear phagocytes such as macrophages and microglial cells can contribute both to the formation and resolution of neuroinflammatory lesions. They do so because they shift their molecular characteristics and functional properties as lesions evolve. Here we want to dissect the immune cell- and nervous system-derived signaling streams that govern phagocyte phenotypes in the inflamed CNS.

Project-related publications

de la Rosa C, Kendirli A, Baygün S, Bauernschmitt F, Thomann AS, Kisioglu I, Beckmann D, Carpentier Solorio Y, Pfaffenstaller V, Tai YH, Mehraein N, Sanchez P, Spieth L, Gerdes LA, Beltran E, Dornmair K, Simons M, Peters A, Schmidt-Supprian M, Kerschensteiner M. (2026) In vivo CRISPR screen reveals regulation of macrophage states in neuroinflammation. Nat Neurosci. 29(2):493-509.

Jordão MJC, Sankowski R, Brendecke SM, Sagar, Locatelli G, Tai YH, Tay TL, Schramm E, Armbruster S, Hagemeyer N, Groß O, Mai D, Çiçek Ö, Falk T, Kerschensteiner M, Grün D, Prinz M. Single-cell profiling identifies myeloid cell subsets with distinct fates during neuroinflammation. Science 2019 Jan 25;363(6425):eaat7554

Locatelli G, Theodorou D, Kendirli A, Jordão MJC, Staszewski O, Phulphagar K, Cantuti-Castelvetri L, Dagkalis A, Bessis A, Simons M, Meissner F, Prinz M, Kerschensteiner M. Mononuclear phagocytes locally specify and adapt their phenotype in a multiple sclerosis model. Nat Neurosci. 2018 Sep;21(9):1196-1208.

Goldmann T, Wieghofer P, Jordão MJ, Prutek F, Hagemeyer N, Frenzel K, Amann L, Staszewski O, Kierdorf K, Krueger M, Locatelli G, Hochgerner H, Zeiser R, Epelman S, Geissmann F, Priller J, Rossi FM, Bechmann I, Kerschensteiner M, Linnarsson S, Jung S, Prinz M. Origin, fate and dynamics of macrophages at central nervous system interfaces. Nat Immunol. 2016 Jul;17(7):797-805.

While white matter lesions dominate the early stages of multiple sclerosis, the gray matter takes center stage as the disease advances. We thus try to better characterize gray matter pathology in multiple sclerosis patients, develop models that allow us to address distinct aspects of gray matter pathology and thereby aim to resolve pathological targets, biological markers and emerging therapies for MS progression.

Project-related publications

Ullrich Gavilanes EM, Bartos LM, Gernert JA, Carral CA, Ruiz Navarro D, Havla J, Gerdes LA, Gnörich JS, Kunze LH, Dorneich JS, Pakula V, Tagnin L, Zimmermann H, Seelos K, Franzmeier N, Frontzkowski L, Pedrosa de Barros N, Ribbens A, Zwergal RM, Zwergal A, Vollmar C, Remi J, Picon C, Reynolds R, Merkler D, Wattjes MP, Kümpfel T, Brendel M, Kerschensteiner M. (2025) SV2A-PET imaging uncovers cortical synapse loss in multiple sclerosis. Sci Transl Med. 17(818):eadt5585.

Jafari M, Schumacher A-M, Snaidero N, Neziraj T, Ullrich Gavilianes EM, Jürgens T, Florez Weidinger JD, Schmidt SS, Beltran E, Hagan N, Woodworth L, Ofengeim D, Gans J, Wolf F, Kreutzfeldt M, Portugues R, Merkler D, Misgeld T, Kerschensteiner M. Localized calcium accumulations prime synapses for phagocyte removal in cortical neuroinflammation. Nat Neurosci. 2021 Mar;24(3):355-367.

Jürgens T, Jafari M, Kreutzfeldt M, Bahn E, Brück W, Kerschensteiner M, Merkler D. Reconstruction of single cortical projection neurons reveals primary spine loss in multiple sclerosis. Brain 2016 Jan;139(Pt 1):39-46.

February 2026 – Here the Kerschensteiner lab developed a new CRISPR-based in vivo screening platform that reveals how cytokines orchestrate macrophage behavior in multiple sclerosis. By editing progenitor cells before transplantation, they mapped how key immune signals—like IFN-γ, TNF, GM-CSF, and TGF-β—shape myeloid cell migration, phagocytosis, and activation inside the brain. The approach combines single-cell profiling and biosensors to visualize immune dynamics in real time, offering an unprecedented window into the molecular regulation of myeloid cells in neuroinflammation.

LINK zu SyNergy Research Spotlight: https://www.synergy-munich.de/news-events/news/in-vivo-crispr-screen-reveals-regulation-of-macrophage-states-in-neuroinflammation/d7f59c6dcb958f7d

LINK zu BMC News Feature: https://www.med.lmu.de/bmc/en/news/latest-news/news-overview/news/in-vivo-crispr-screen-reveals-regulation-of-macrophage-states-in-neuroinflammation-aaa223d5.html

October 2025 – Gray matter damage and cortical lesions drive progression in people with multiple sclerosis (PwMS). In a new study, the Kerschensteiner lab collaborated with our clinical team and the group of Matthias Brendel at the Department of Nuclear Medicine to show that positron emission tomography (PET) imaging of the synaptic vesicle protein 2A (SV2A) can reveal early synapse loss in MS. After validating SV2A as a marker of synapse density in cortical tissue and a mouse model of cortical MS, the team used SV2A-PET in 31 PwMS and detected in vivo synapse loss in cortical lesions. Interhemispheric differences in tracer uptake uncovered extensive cortical synapse pathology, exceeding MRI-visible cortical lesion volume by more than 20-fold. These PET-defined regions were larger in progressive MS and correlated with disability and cognitive performance, indicating that SV2A-PET exposes clinically relevant cortical pathology that remains invisible to conventional MRI and offers a promising tool to monitor MS progression.

LINK zu SyNergy Research Spotlight: https://www.synergy-munich.de/aktuelles/news/using-pet-imaging-to-detect-cortical-synapse-loss-in-multiple-sclerosis/4fb10532e49e8b46

LINK zu BMC News Feature: https://www.med.lmu.de/bmc/en/news/latest-news/news-overview/news/using-pet-imaging-to-detect-cortical-synapse-loss-in-multiple-sclerosis-b938def0.html

April 2025 – Meningeal lymphoid follicles (eLFs) are detected in many people with severe MS but their function is unclear. Here, the Peters lab together with the Kawakami, Beltrán and Kerschensteiner labs investigated the cellular processes inside eLFs in a model system, and could show for the first time that B and T cells form long-lasting contacts in these structures. These interactions lead not only maturation of B cells, but also to reactivation of autoreactive T cells and could thereby fuel chronic inflammatory processes in the CNS during MS.

September 2024 – Here the Gerdes lab together with the Beltran lab analyzed CD8 T cells from the blood and cerebrospinal fluid of monozygotic twins, where one twin had MS and the other showed no signs or subclinical signs of neuroinflammation (SCNI). The Study demonstrates that CD8 T cells from twin with MS and cotwin with SCNI displayed proinflammatory immunological and metabolic features consistent with enhanced activation and migration. This provides insights about CD8 T cells in MS progression. Read more.

April 2024 – Membrane damage is key step in the pathological cascade that leads to neuronal death or axon degeneration. Here, the Kerschensteiner lab worked together with a research team headed by Oliver Thorn-Seshold at the LMU Department of Pharmacy to develop new modular fluorogenic probes that reveal the whole cytosolic volume of damaged cells, with near-zero background fluorescence. We identify a specific disulfonated fluorogenic probe type that only enters cells with damaged membranes, then is enzymatically activated and marks them. By showing that these fluorescent probes can label membrane damaged neurons in vitro and in vivo we provide a powerful new tool for wash-free in vivo imaging of membrane damage and outline chemical designs that may be adapted for the selective delivery of drug cargos to damaged neurons.

October 2023 –The infiltration of autoreactive T cells to the central nervous system (CNS) triggers lesion formation in the common neuroinflammatory condition multiple sclerosis (MS). Here, the Kawakami and Kerschensteiner labs worked together to provide a comprehensive characterization of the essential molecules that regulate this transmigration process. By performing a genome-wide CRISPR screen in a rat MS model they could identify 18 essential facilitators of T cell migration to the CNS. These can be grouped into three functional modules that regulate T cell adhesion, chemotaxis and egress. Notably, many of these molecules show regulated expression in T cell from MS patients and include prominent targets of approved MS therapies.

Kendirli A, de la Rosa C, Lämmle KF, Eglseer K, Bauer IJ, Kavaka V, Winklmeier S, Zhuo L, Wichmann C, Gerdes LA, Kümpfel T, Dornmair K, Beltrán E, Kerschensteiner M*, Kawakami N* (2023) A genome-wide in vivo CRISPR screen identifies essential regulators of T cell migration to the CNS in a multiple sclerosis model. Nat Neurosci. 26(10):1713-1725.

Press release : https://www.lmu.de/en/newsroom/news-overview/news/identified-key-regulators-involved-in-genesis-of-multiple-sclerosis-lesions.html

August 2023 – Inflammation in the central nervous system can impair the function of neuronal mitochondria, the energy-producing components within nerve cells, which contributes to axonal degeneration in multiple sclerosis (MS). Here the Kerschensteiner lab at LMU Munich and the Misgeld lab at TU Munich have teamed up to unravel how inflammation changes the molecular composition and functional capacity of neuronal mitochondria. This work identifies the TCA cycle as new potential target for therapeutic interventions to protect nerve cells in MS.

Press release Synergy: https://www.synergy-munich.de/news/news/kerschensteiner-misgeld/index.html

April 2023 – In multiple sclerosis immune-mediated myelin loss can be partially reversed by remyelination. Here the Kerschensteiner lab and the Misgeld lab at TUM investigate if and how mature oligodendrocytes that survive in the lesion area in both MS patients and models can contribute to the myelin repair process. In a mouse model of cortical MS pathology they show that while surviving oligodendrocytes can extend new proximal processes they rarely form new myelin internodes. Furthermore drugs that boost myelin recovery by targeting oligodendrocyte precursor cells did not enhance myelin repair by surviving oligodendrocytes indicating that distinct therapeutic approaches are required to recruit surviving oligodendrocytes to the remyelination process.

November 2021 – Progressive multifocal leukoencephalopathy (PML) is a severe CNS infection that can occur in MS patients treated with Natalizumab. Clinical management of patients with Natalizumab-associated PML is challenging not least to detect, monitor and differentiate PML lesions are limited. Here the Kerschensteiner lab and Kümpfel group teamed up to investigate whether TSPO PET imaging can be applied to monitor the inflammatory activity of PML lesions over time. The results of this monocentre pilot study now indicate that TSPO PET imaging may faciliate longitudinal monitoring of disease activity and help distinguish recurrent multiple sclerosis activity from PML progression.

January 2021 – Gray matter pathology is a critical contributor to disability in advanced stages of multiple sclerosis. Here the Kerschensteiner lab teamed up with the Misgeld and Merkler lab to investigate how neuronal structure and function is impacted in the neuronal gray matter. In a mouse model they show that gray matter inflammation leads to a synapse loss that is accompagnied by neuronal silencing and can be reversible. Synapse loss is primed by local calcium increases, executed by activated microglial cells and infiltrating monocyte-derived macrophages and can be mitigated by therapeutic strategies that interfer with pathological activation of phagocytes. The authors hope that their work can help the development of therapeutic approaches that curb progression in MS patients.

September 2020 – To interrogate the rules that govern myelin replacement in the cortex the Kerschensteiner group together with the Misgeld lab at TUM studied the response to the ablation of single cortical oligodendrocytes. Using timelapse imaging and correlated ultrastructural reconstructions they were able to show that a loss of a single oligodendrocyte is sufficient to cause robust cell and myelin replacement. In this process internodes along partially myelinated axons were typically not reestablished, while myelin sheaths forming continuous patterns showed remarkable homeostatic resiliences and remyelinated with single axon precision. Understanding these principles is particularly important in the context of multiple sclerosis which extensive cortical demyelination is a major pathological feature and target of remyelination therapies.

Februar 2019 – To reveal the mechanisms that drive inflammatory axon degeneration the Kerschensteiner lab has used in vivo calcium imaging in a multiple sclerosis model. Dynamic tracking of individual axons in the inflamed spinal cord shows that cytoplasmic calcium levels determine the choice between axon loss and survival. Calcium can enter the axon through nanoscale ruptures of the axonal plasma membrane that are induced in inflammatory lesions. These results thus identify a unusual axon injury pathway that can contribute to neurodegeneration in multiple sclerosis and may represent a novel target for protective therapy.

Press Release

Februar 2018 – Mononuclear phagocytes can both promote and inhibit inflammation. Here the Kerschensteiner lab uses an in vivo imaging approach to follow the evolution of phagocyte phenotypes in neuroinflammatory lesions. By tracking phagocytes over time they can show that individual phagocytes switch their phenotype as lesions move from expansion to resolution. This phenotype shift appears to be initiated by signals derived from the nervous system tissue. Understanding the molecular nature of these signals might thus provide the basis for therapeutic manipulation of phagocyte function in the inflamed CNS.

Press Release

November 2016 – Damage to oligodendrocytes and their myelin sheaths is a central feature of multiple sclerosis pathology. Here the Kerschensteiner lab investigates how oligodendrocyte damage is initiated in multiple sclerosis (MS) and EAE using in vivo imaging, confocal microscopy as well as electron microscopy. They can show that oligodendrocyte damage spreads centripetally and that the formation of focal myelin outfoldings that they call “myelinosomes” is an early sign of oligodendrocyte damage both in MS and EAE…

January 2016 – How neurodegeneration starts in the brains of progressive multiple sclerosis patients is only incompletely understood. Here the Kerschensteiner lab joined forces with the Merkler lab at the University of Genevan and used confocal microscopy of Golgi-Cox impregnated tissue sections to reconstruct single cortical projection neurons in brain sections from multiple sclerosis and control patients. Their study reveals a widespread and pronounced loss of dendritic spines that occurs independently of cortical demyelination and axon loss and indicates the presence of a primary synaptic pathology in multiple sclerosis…

December 2014 – The loss of axonal connectivity underlies the devastating consequences of spinal cord injuries. Here the Misgeld lab at TUM and the Kerschensteiner lab use spinal in vivo imaging to show that axons persist in a metastable state for hours after spinal contusion injury. During this time the intra-axonal calcium dynamics determine the axonal fate. Those axons that manage to re-establish calcium homoestasis will survive ong term while those that fail to do so will degenerate. This study identifies an inherent self-preseravtion process in contused axons and a window of opportunity for rescuing axonal connectivity after contusion injury.

December 2014 – The axonal transport of cargos from the neuronal cell body to the synapse (and back) is key for maintaining neuronal health and function. Here the Kerschensteiner lab visualizes the dynamics of organelles in individual spinal axons and reveals widespread impairment of organelle transport in MS models. Transport deficits precede structural alterations of axons, myelin or microtubules. They persist in chronic MS models and lead to a reduced distal organelle density – a possible first step towards axonal degeneration.

May 2014 – Mitochondria the main energy source of the cell play a key role in neuronal physiology and pathology. Here the Misgeld (TUM) and Kerschensteiner (LMU) labs establish a novel multiparametric imaging approach that allows to visualize and mechanistically dissect mitochondrial redox signals with high temporal and spatial resolution in the living nervous system. This new technique thus offers new dynamic insights into mitochondrial signaling in the healthy or diseased nervous system.

Daniela Beckmann, PhD student

I studied Molecular Medicine at Ulm University in a Bachelor- and consecutive Master programme. During this time, I became particularly interested in both neuroscience and immunology, which is why I happily ended up as a PhD student in Neuroimmunology and joined the Kerschensteiner Lab in October 2019. I study the calcium-mediated process of axon degeneration in inflammatory lesions, using transgenic and in vivo imaging techniques. To pursue this PhD project, I was awarded a scholarship by the “Studienstiftung des deutschen Volkes” (German Academic Scholarship Foundation). Whenever I am not in the lab, you will find me playing clarinet in a symphonic wind orchestra or reading a good book.

Clara de la Rosa del Val, PhD student

I studied Biochemistry at the Autonomous University of Madrid, in Spain, doing a one-year exchange at the University of Toronto, Canada. I really liked the international experience, so for my master I decided to move abroad to Munich. I studied a MSc of Neuroscience with the Graduate School of Systemic Neurosciences (GSN) at the Ludwig-Maximilians Universität. During my master studies, I already joined the Kerschensteiner Lab, first for a research internship and later for the Master Thesis. Now I’m continuing with the PhD, also as part of the GSN. I work on the functional regulation of phagocytes and T cells in neuroinflammation, using the CRISPR/Cas9 technology in CRISPR screens. In my free time, I like to read, paint, hike and go to the Alps (hands down one of the best things about Munich), read some more and have fun with friends.

Emily Melisa Ullrich Gavilanes, Post-doctoral fellow

Born and raised in Quito, Ecuador, I moved to Germany for my bachelor’s degree in Biochemistry and Cell Biology at Jacobs University Bremen. I then obtained a Master in Cellular and Molecular Neuroscience at Karl Eberhardt Universität Tübingen before moving to Munich to work on my PhD in the Kerschensteiner lab in November 2018. My project focuses on the mechanisms that lead to grey matter spine and neuron loss in a model of cortical multiple sclerosis. Outside of the lab I enjoy spending my time doing sports like skiing, tennis, swimming or I enjoy nice days with walks around the city parks and lakes.

Dr. Yi-Heng Tai, Postdoctoral fellow

After my master’s training in brain science in Taiwan, I did my PhD here focusing on the mitochondrial pathology in an immune-mediated neurodegenerative model. It is quite fascinating to make great effort on staring at this tiny subcellular structure- imagine how important this organelle is and how they affect your life (#powerhouseisonfire hashtag years spent for my PhD). Coming from subtropics, I fell deeply in love with the winter here in Munich. The alps also made me an ‘’outdoor person’’. No doubt that I hike and enjoy the beer on top of the mountain. Apart from outdoor activities, I travel, cook and bake (like a lot). And just fyi- if you would like to bring some sweets for me, I am a Krapfen lover!

Nils Treiber, MD student

I have been studying medicine at the LMU/TUM since 2018 and got to the Kerschensteiner lab initially through the `LMU-Forschungsmodul´ as an intern. Since then I have been introduced to great many techniques and surgeries while helping to research progressive MS models. After my preclinical phase I will be doing my MD on my current subject of progressive forms of MS. In my medical studies I was always fascinated by neurological disease, which is why I am excited to contribute to better understanding them. I originally come from a rather small town near the alps, which is why I really enjoy going hiking and skiing, knowing the secret tips. In the rest of my free time I also like working and troubleshooting (Pfusch) on my old car, playing dungeons and dragons with friends and riding my (slightly too fast) bike.

Ionna Emmanouilidis, PhD student

I studied Biology at Pierre and Marie Curie University in Paris and spend a semester abroad at Karolinska Institute in Stockholm. I moved to Munich to study at the Graduate School of Systemic Neurosciences and obtained an MSc of Neuroscience. I joined the Kerschensteiner lab in October 2019 for a short internship, which turned into a master thesis, which then turned into a PhD project that I do in both the Kerschensteiner and the Misgeld lab (Technical University of Munich). My PhD project´s aim is to reveal the mechanisms underlying plasma membrane repair in porated axons in the context of neuroinflammation and spinal cord contusion injury. To address this question I use methods such as in vivo 2-photon imaging and CRISPR manipulations. Born and raised in Greece I prefer the sea over the Bavarian Alps and summer over winter. I spend a lot of my free time reading or discovering the city with my friends, so ask me if you ever need `where to go in Munich´ advice.

Veronika Pfaffenstaller, PhD student

I studied Biology and the consecutive Master Human Biology - Principles of Health and Disease at the Ludwig-Maximilians Universität München. I joined the Kerschensteiner lab for a research internship and later for my Master Thesis. I will continue with my PhD working on identifying new therapeutic target structures for the modulation of phagocyte function in neuroinflammation and to validate them functionally, molecularly and pharmacologically using the CRISPR/Cas9 technology. Outside the lab, I enjoy sports like running, swimming and ballet, or I like reading and playing dungeons and dragons with friends (yes we also have a lab dnd group).

Yves Carpentier Solorio, PhD student

Born in Mexico and raised in Montreal, Canada, I did a bachelor and a master’s degree in Neurosciences at the University of Montreal. I joined the Kerschensteiner lab in September 2022 to do my PhD to pursue my interest in neuroimmunology. My project focuses on the mechanisms of axonal degeneration in the spinal cord in a mouse model of MS using CRISPR/Cas9 technology. During my free time, you can find me on a tennis court, cooking or simply on my couch with a charcuterie board and a rosé.

Victoria Böck, Institute Technical Assistant

I was born in Munich and i still love to live in the capital of bavaria. After secondary school i did an apprentice ship to become a MTLA (medical-technical-laboratory-assistant), which i completed with a state examination. I worked in a routine microbiology lab for a few years before moving into research. My first research experience was in biochemistry and molecular biology, after which I switched to neuroimmunology, into the Institute of clinical neuroimmunology, where I really enjoy working. In my free time, I try to be outside as much as possible, for example riding my motorcycle, travel around the world or hiking in the mountains. At home I sew myself useful things or read technical literature.

Carla Ares Carral, PhD student

Made in Spain. After getting my bachelors degree in Biochemistry at the Universidad Complutense de Madrid, I moved to München because I heard beers and the Alps were nice. Now I can say… combined are better. After doing a research internship at Kerschensteiner lab as part of the LMU Human Biology - Principles of Health and Disease Master Program, I decided I enjoyed it too much not to stay. First it was just for the master thesis. Now for a PhD, which focuses on the identification of molecular signals that mediate adaptive instruction of innate effector function in MS. When I’m not bothering my coworkers at the BMC, you’ll probably find me running around the city, grabbing coffee with friends or making tortilla de patata.

Anastasiia Sydorenko, MD student

Born and raised in Ukraine, Kiew, I moved to Munich to study biochemistry (TUM). During my bachelor’s a wish to combine both fascination in science and direct patient’s care led to my decision to study medicine (LMU) while continuing with my master’s in biochemistry (TUM). Having developed a strong interest in both neurobiology and immunology I joined the Kerschensteiner Lab first for a research internship during my master’s and I am now happy to be back for my medical thesis. To pursue my MD I was awarded a scholarship by the Hertie foundation. In my project I study the role of pyroptosis players gasdermin D and E in the axon degeneration in inflammatory lesions of a mouse model of multiple sclerosis using transgenic and in vivo imaging. Whenever I'm not in the lab, I enjoy sports like hiking, climbing and skiing (well, still learning it, but being passionate), dancing (ballet and modern), acting in an amateur theater or just reading a good book.

I started to get interested in neuroimmunology early on in my medical studies. Therefore I moved from Aachen to Munich to join Hartmut Wekerle`s department at the Max Planck Institute for Neurobiology, where I worked for 6 years in parallel to my medical studies. At the time it became clear that axonal injury was a critical determinant of disability in MS patients and I wanted to learn more about neuroscientific approaches to axonal pathology. Supported by a postdoctoral fellowship I therefore joined the lab of Martin Schwab at ETH Zurich and developed first targeted EAE models that allowed the induction of neuroinflammatory lesions in a defined axonal tract system (and subsequent analysis of axonal injury and compensation).

During this time I also visited a friend of mine (Thomas Misgeld), then a post doc in Jeff Lichtman`s lab at Washington university in St. Louis, and we managed to obtain first in vivo images of fluorescently labeled axons in the spinal cord. Based on this we were able to secure funding that allowed me to join Jeff`s lab first at Wash U and then at Harvard and enabled us to establish imaging strategies to study axonal pathology in real time. Support from the Emmy Noether program of the DFG then made it possible for me to start my own research group at the Institute of Clinical Neuroimmunology of the LMU Munich. Since then I have tried to apply dynamic imaging approaches to better understand the cellular and molecular interactions that determine the fate of neuroinflammatory lesion, first as a group leader, then as an associate professor and since 2013 as full professor.

As the director of the Institute of Clinical Neuroimmunology I hope to be able to continue the groundbreaking work of my mentors Reinhard Hohlfeld and Hartmut Wekerle and aim to provide an environment that stimulates scientific independence and creativity and hopefully contributes to meaningful improvements of our understanding of neuroinflammatory conditions and our means to diagnose, monitor and treat them.

Person

Name: Prof. Dr. med. Martin Kerschensteiner

Education and Academic Appointments

Since 2013 Full professor and Director of the Institute of Clinical Neuroimmunology, Medical Center of the LMU Munich

2008 – 2013 Associate Professor for Translational Neuroimmunology at the Institute of Clinical

2005 – 2008 Group leader funded by the Emmy Noether-Program of the German Research Foundation (DFG), Institute of Clinical Neuroimmunology, Medical Center oft he Ludwig-Maximilians-University Munich (LMU Munich)

2004 – 2005 Research Associate in the Department of Molecular and Cellular Biology (lab of Prof. J. Lichtman), Harvard University, Cambridge, USA

2003 – 2004 Research Associate in the Department of Anatomy and Neurobiology (lab of Prof. J. Lichtman), Washington University School of Medicine, St. Louis, USA

2001 – 2003 Post-doctoral fellow in the Department of Neuromorphology (director: Prof. M. Schwab), Brain Research Institute, University and ETH Zurich, Switzerland

1999 – 2001 Residency training in Neurology, University Hospital LMU Munich

2000 Medical degree (Dr. med.; summa cum laude)

1994 – 1999 MD thesis at the Department of Neuroimmunology (director: Prof. H. Wekerle), Max-Planck-Institute of Neurobiology, Martinsried

1992 – 1999 Medical Studies at the RWTH Aachen and the LMU Munich

Coordinating Functions

Since 2020 Deputy Speaker of the Collaborative Research Center SFB-TRR 274 “Checkpoints of CNS recovery”

Since 2020 Head of the Examination Board, Elite Master Program “Human Biology –Principles of Health and Disease”, LMU Munich

Since 2017 Deputy Chair of the Biomedical Center of the LMU Munich

Since 2016 Board Member of the Clinical Compentence Network “Multiple Sclerosis”

Since 2016 Board Member of the Collaborative Research Center SFB-TRR 128 “Multiple Sclerosis –Initaiting/effector vs. regulatory mechanisms”

Since 2012 Board Member and Research Focus Coordinator of the Excellence Cluster “Munich Cluster for Systems Neurology (SyNergy)”

Awards and Honors