Prize Winners 2023: Award for research on Rett syndrome

Botond Roska and José-Alain Sahel honored with the International Prize for Translational Neuroscience for developing treatment for hereditary blindness

Blind people may one day be able to see again. Research has come a big step closer to this goal, which sounds like a biblical miracle, in recent years. This year, the Gertrud Reemtsma Foundation is awarding the International Prize for Translational Neuroscience to two scientists who have laid the groundwork. Botond Roska of the Institute of Molecular and Clinical Ophthalmology Basel has genetically modified cells in the retina of the eye to take over the function of defective sensory cells. José-Alain Sahel of Sorbonne University in Paris has developed a gene therapy for patients and light-enhancing glasses as a visual prosthesis. A patient who had gone blind decades ago was able to perceive light stimuli from his environment again thanks to the treatment.

Hereditary or age-related defects of the retina are often the cause of eyesight loss. Retinitis pigmentosa is one of the most common hereditary retinal diseases, affecting more than two million people worldwide. Various mutations cause the sensory cells of the retina to degenerate. Except for one approved gene therapy in rare early onset condition, it has not yet been possible to restore sight to people who are already blind. A tiny green alga has shown research new ways towards a therapy for this disease. Chlamydomonas reinhardtii consists of only one cell and has no eyes. But thanks to light-sensitive proteins, the alga can still move toward the light. These proteins, known as channelrhodopsins, are similar to the light-sensitive molecules in human sensory cells in the eye. Researchers have inserted the genes for the channelrhodopsin into other cells, making them light-sensitive. This technique, known as optogenetics, has provided many new insights in neuroscience. Its use is also being explored for the treatment of deafness.

Restoring vision in mice and humans

Botond Roska has studied the functions of different cell types in the retina and the effects of genetic defects in these cells. He developed a method that allows him to insert genes into the genome of specific cell types using harmless viruses. In this way, Roska has succeeded in restoring vision in blind mice and human retina. In order to test the technique on humans, José-Alain Sahel developed a gene therapy for humans. Sahel is an ophthalmologist researching new drug therapies, retinal prostheses, and gene therapies to treat hereditary or age-related defects of the retina. For one clinical trial, researchers treated a patient with retinitis pigmentosa who had gone blind more than a decade ago. The team inserted a gene for the light- sensitive molecule Chrimson R into the patient’s retina. This made retinal ganglion cells, which naturally cannot receive optical signals, light-sensitive. It took nearly five months for the cells to produce the protein permanently and for the patients to start interpreting the signals. Chrimson R reacts only to a small part of the spectrum of the visible light, namely yellow-orange light. However, this is not sufficient to adequately perceive the environment under normal lighting conditions. The team led by José-Alain Sahel therefore developed light-enhancing glasses that record the surroundings with a camera, convert the signals into the respective wavelengths and transfer them to the patient’s retina in real time. Intensive training was required for the patient to see with the special glasses. After seven months, he could locate, touch and count objects in front of his eyes. These findings have been now observed in other patients in this trial. Measurements of brain activity showed that the visual center in the brain was activated in the process. The results show that optogenetic therapy can at least partially restore vision in people with retinitis pigmentosa. However, before the treatment can be used in clinics, it must first be tested and optimized in further studies.

The award winners

Botond Roska first studied cello and mathematics in Budapest. He then obtained his M.D. at the Semmelweis Medical School, a Ph.D. in neurobiology from the University of California, Berkeley and studied genetics and virology as a Harvard Society Fellow at Harvard University and the Harvard Medical School. He then led a research group at the Friedrich Miescher Institute in Basel from 2005-2018. In 2010 he became Professor at the Medical Faculty and in 2019 Professor at the Science Faculty of the University of Basel. Since 2018 he is a founding director of the Institute of Molecular and Clinical Ophthalmology Basel. There, he leads a research group focusing on the understanding of vision and its diseases and the development of gene therapies to restore vision. José-Alain Sahel studied medicine in Paris and became an ophthalmologist at Louis Pasteur University Hospital in Strasbourg in 1984. After a fellowship at the Massachusetts Eye and Ear Infirmary, Harvard Medical School, and a visiting scholarship at Harvard University, he became a Professor of Ophthalmology at Louis Pasteur University in Strasbourg in 1988, and in 2002 at Sorbonne University in Paris, and University College London. He founded the Vision Institute in Paris in 2008 and directed it until 2021. Since 2023 he is professor emeritus at Sorbonne University. Since 2016 he is endowed Distinguished Professor and Chairman of the Vision Institute at the University of Pittsburgh Medical Center.

Prize Winners 2022: Award for research on Rett syndrome

Huda Zoghbi and Adrian Bird receive the International Prize for Translational Neuroscience for their findings on the causes of Rett syndrome

The brain is one of nature’s most complex structures. About 100 billion nerve cells work together to control vital functions as well as thinking and learning processes. When it comes to neurological diseases, it is often quite difficult to uncover the underlying changes. This year, the Gertrud Reemtsma Foundation is awarding the International Prize for Translational Neuroscience to two scientists for their work on Rett syndrome. Huda Zoghbi from the Baylor College of Medicine in the US has identified the MECP2 gene as the cause of Rett syndrome and studied its role in various neurons. Adrian Bird from the University of Edinburgh has uncovered the role of the MECP2 protein in the regulation of genes and genetically modified mice so that Rett syndrome can be researched in them. The two researchers have thus made a substantial contribution to better understanding the disease and creating the basis for new treatment options. The prize will be awarded on 16 June 2022 at the Bucerius Kunst Forum in Hamburg. Parents are usually the first to notice that something is wrong. A previously healthy toddler suddenly seems to have lost interest in their fellow human beings and the environment. First learned words disappear, and the child has difficulties with walking and balance. Rett syndrome is a neurological disorder that includes various symptoms such as autism, epilepsy, and anxiety. Every year, about 50 children in Germany – primarily girls – are affected by this disease. After a normal first year of life, those affected increasingly lose their ability to speak and move. This makes them dependent on care throughout their lifetime. Rett syndrome is often characterized by repetitive hand movements reminiscent of hand washing. The patients sometimes show strong autistic traits and suffer from anxiety and multiple physical symptoms such as breathing problems or spinal curvature. There is still no treatment for this serious disease. When Huda Zoghbi diagnosed Rett syndrome in two girls within a short time at the beginning of her neurology training in 1983, relatively little was known about the disease. Zoghbi wanted to find the trigger of this complex disease. Because only one family member is affected at a time, spontaneously occurring changes in the genetic make-up seem to be the cause. Finding the gene responsible for this was an enormous challenge at the time – also because genetic analyses were still quite time-consuming and expensive. For more than 10 years, Zoghbi studied the genetic material of the affected families and gradually narrowed down the possible genes. She finally found changes in a gene called MECP2 on the X chromosome in people with Rett syndrome. These mutations result in the production of a defective MeCP2 protein and thus trigger the disorder. The MeCP2 protein was discovered a few years earlier by Adrian Bird. The scientist found that MeCP2 binds to specific sites on the DNA that are marked with methyl groups and can thus modulate expression of thousands of genes in neurons. MeCP2 thereby optimises levels of gene expression. When it became known that many nerve cells in patients with Rett syndrome were unable to produce a functioning MeCP2 protein, Bird decided to investigate the its role in these cells in more detail. He developed genetically modified mice in which the MECP2 gene is switched off. These mice have typical characteristics of Rett syndrome and form an important basis for research into the disease. The fundamental findings of Zoghbi and Bird made it possible to study the unusual clinical picture of Rett syndrome in greater detail. Affected children initially develop normally because MeCP2 is needed in higher concentrations in the nerve cells only from the second to third year of life. An absence therefore does not have a negative effect during this time. However, with increasing age, the lack of MECP2 drastically alters the transmission of stimuli in the nerve cells, and the first impairments start to appear. The disease occurs mainly in girls because they have two copies of the X chromosome. Females silence one entire X chromosome early in development. As they are heterozygous for the disease mutation, this leads half their cells shutting down the normal gene, while the other half silence the chromosome carrying the mutant gene. The latter cells are normal with respect to MeCP2 function. Females with these mutations are rescued by X inactivation, but at the price of Rett syndrome. In male babies, on the other hand, all the nerve cells are damaged. They therefore usually die before or shortly after birth. Huda Zoghbi and Adrian Bird are also trying to develop treatments that could improve the lives of Rett patients. Using the genetically modified mice, Zoghbi found that stimulating brain regions – using technology applied in in Parkinson’s therapy – can correct deficits in learning and memory. Exercise and brain training of the mice before the onset of symptoms also mitigates the course of the disease. Bird reactivated the production of MeCP2 in the nerve cells in the genetically modified mice. The mice that had already shown considerable impairments recovered and became almost completely healthy. This shows that this neurological disease is reversible and gives hope that Rett syndrome can one day be cured.

The prize winners

Huda Zoghbi studied biology and medicine at the American University of Beirut, Lebanon and received her doctorate in medicine from Meharry Medical College, Nashville, Tennessee in 1979. She then went on to Baylor College of Medicine and Texas Children’s Hospital, Houston, Texas, where she trained in Pediatrics and Neurology, and then pursued postdoctoral research in molecular genetics. She became Professor of the Department of Pediatrics, Neurology, Neuroscience and Molecular and Human Genetics at Baylor in 1994, and an Investigator with the Howard Hughes Medical Institute in 1996. Since 2010, she has also been the Director of the Jan and Dan Duncan Neurological Research Institute at Baylor College of Medicine and Texas Children’s Hospital.

Adrian Bird studied biochemistry at the University of Sussex and obtained his PhD from the University of Edinburgh in 1971. He then had research residencies at the University of Zurich, Switzerland and Yale University. In 1975, he set up his own research in Edinburgh. From there, he went to the Institute of Molecular Pathology in Vienna, where he stayed from 1987 to 1990. In 1990, he returned to the University of Edinburgh, where he has held the Buchanan Chair in Genetics ever since.

Prize Winners 2021: Award-winning diagnosis of brain tumours

Hai Yan and Andreas von Deimling have been awarded the International Prize for Translational Neuroscience 2021

Cancer cells multiply uncontrollably, thereby displacing healthy cells and destroying tissue. But that’s where the similarities end. Uncontrolled cell division can have various causes, and the individual cancers must therefore be treated accordingly. The more precisely the characteristics of the respective cancer cells are known, the more specifically the malignant cells can be combated.

Until now, brain tumours had been classified mainly by staining tissue samples and comparing the appearance under a microscope. However, the origin and molecular characteristics of cancer cells, which are often decisive for further therapy, are not always visible with this type of diagnostics. It had therefore not been possible to distinguish between the different tumour types in some cases.

Hai Yan has researched the characteristics of the most common types of brain tumours: gliomas. Sub-forms of these incurable glial cell tumours form typically modified proteins. IDH1 and IDH2 have been found by his team and his collaborators to be frequently altered with an amino acid replaced at a specific position in certain types of gliomas. This distinguishes tumour cells from normal body cells as well as from other tumour sub-types in which the proteins are present in their natural form.

Hai Yan found that one sub-group of gliomas can be simply distinguished from others by looking at the distribution of the commonly mutated proteins. He and his collaborators identified diagnostic biomarkers that significantly improve the differentiation of these sub-groups. The World Health Organisation has included the tumour types they discovered in the classification of tumours of the central nervous system. Yan and his team also investigated how the altered proteins affect the metabolism and immortality of the tumour cells. Tailored therapies against these forms of glioma are based on these findings.

Andreas von Deimling also works on diagnostic markers of brain tumours. He and his team have developed an antibody that binds to mutated IDH1 protein. The highly specific antibody recognizes the mutation and binds to the protein only when exactly this mutation is present. It had previously not been possible to distinguish between normal and mutated IDH1 using conventional staining methods.

With the help of the antibody, sub-types of gliomas – astrocytomas and oligodendrogliomas – can be diagnosed beyond doubt and differentiated from other types of brain tumours. The patented antibody is now routinely used worldwide in brain tumour diagnostics. With the help of this antibody, researchers can visualize the tumour cells and their immediate surroundings in the brain tissue. This has already allowed important insights into the development and progression of these tumour diseases.

Von Deimling and his colleagues have also developed a diagnostic system based on the DNA methylation pattern in the tumour cells. These chemical modifications in the genetic material can be used to determine from which cell type a tumour originally arose. In the highly modified cancer cells, this can often no longer be clearly determined. However, knowing the origin is important for designing an effective therapy against the malignant cells.

Prize Winners 2020: Award for excellence in Alzheimer research

Roy Weller, Maiken Nedergaard, and Mathias Jucker honoured for their findings on brain cleansing and its importance in dementia

Alzheimer’s disease is the most common form of dementia and affects at least 50 million people worldwide. The progressive death of nerve cells is associated with the deposition of protein aggregations known as amyloid plaques. With increasing age, such aggregations are more difficult to dissolve and remove from the brain. This year, the Gertrud Reemtsma Foundation honours Roy Weller, Maiken Nedergaard, and Mathias Jucker, three neuroscientists who have investigated the removal of waste products from the brain. The researchers’ findings offer new approaches for treatments and preventive measures for Alzheimer’s and other neurodegenerative diseases. The International Prize for Translational Neuroscience of the Gertrud Reemtsma Foundation (previously known as the K.J. Zülch Prize) valued at € 60,000 will be awarded on 10 September 2020 in Cologne.

Cellular waste products are transported into the blood via lymph vessels and nodes, degraded in the liver, and recycled or excreted in the urine. An exception to this is the brain, in which there are no conventional lymph vessels. The brain is nevertheless highly active and consumes around one quarter of the body’s total energy. This enormous metabolic output also produces a considerable amount of waste. If they are not properly removed, the waste products deposit in the brain. This can lead to the death of nerve cells and possibly dementia.

In Alzheimer’s disease, the amyloid β protein (Aβ) is deposited as plaques around nerve cells that suffer damage consequently. In our younger years, such amyloid plaques are only rarely present in our brains. But as we age, these proteins are less effectively removed. Roy Weller from the University of Southampton wanted to find out how waste products are removed from the brain – and why this often fails with increasing age.

His experiments have shown that waste products from the brain are drained via the walls of arteries. In this process, the brain fluid and the waste products it contains flow to the arteries. From there they are transported to the lymph nodes in the neck by the wave-like contraction of the smooth muscle cells in the walls of the arteries. The extremely narrow pathways of this unique system allow proteins and metabolic products to be removed. However, the pathways are too narrow to allow the traffic of immune cells from the brain to lymph nodes. This has a significant effect on immune reactions in the brain.

Because the arteries lose smooth muscle cells over time and stiffen, this drainage becomes less efficient as we get older. Insoluble Aβ protein can block the narrow drainage pathways and thus further impair its removal. Strengthening of smooth muscle cell contractions and the dissolution of the Aβ proteins to ensure the outflow of Aβ could act as the starting point for therapies for the prevention and treatment of Alzheimer’s disease.

Maiken Nedergaard from the Medical Centre of the University of Rochester and University of Copenhagen has researched the major supportive glial cell type in neuronal diseases, the so-called astrocytes. They surround blood vessel with their processes. This create donut-shaped perivascular tunnels that enables cerebrospinal fluid to flow into brain and literally flush waste products, such as Aβ, out of the brain.

Maiken Nedergaard showed that astrocytes play an important role in distributing fluid in the brain. The transport of Aβ is enabled by the dense expression of the water channel, AQP4. Due to the importance of this predominant glial cell type in the brain’s plumping system, she entitled the brain fluid transport the »Glia-lymphatic« or the »glymphatic system«. In essence, brain waste products are transported along the blood vessels to the lymph nodes.

According to Nedergaard, the glymphatic system is mainly active and removing waste products during sleep. As we sleep, astrocytes shrink and allow larger intercellular spaces into which cerebral fluid can penetrate along the blood vessels. From there, Aβ and other waste products can be removed. These findings could be used to develop new approaches to the prevention and treatment of Alzheimer’s disease.

Mathias Jucker from the Hertie Institute for Clinical Brain Research and the German Center for Neurodegenerative Diseases in Tübingen uses the fluids that cleanse the brain to diagnose neurodegenerative diseases. Jucker identified biomarkers for neurodegeneration in the blood and cerebral fluid of genetically modified mice. These results can be transferred to clinical application in humans. For example, in the cerebral fluid of mice that develop Aβ plaques like Alzheimer’s patients, he discovered molecules with which the progression of Alzheimer’s disease can be predicted early on.

Jucker’s studies also suggest that the clearing of Aβ depends on the proper folding of the protein. As is the case with prions, misfolded Aβ trigger the misfolding of other Aβ proteins in a kind of self- reinforcing domino effect. Misfolded proteins can then no longer be cleared. By the time the first neurological symptoms appear, the brain has already been severely damaged because so many amyloid plaques have formed. Many therapies are therefore no longer effective at this time and a preventive therapy is even more important.

Prize Winners 2019: Therapy for muscle weakness

Adrian Krainer and Richard Finkel receive the Prize for their development and testing of a drug for spinal muscular atrophy

Although spinal muscular atrophy is a rare condition, it is the most common gene-related cause of death in children. This year, The Gertrud-Reemtsma Foundation is awarding the K. J. Zülch prize to a scientist and a clinician who have been developing and testing a new drug to combat this condition: Adrian Krainer at the Cold Spring Harbor Laboratory led a research team that developed antisense agents to combat spinal muscular atrophy, and tested them in mice. These tests met with such success that they led to testing of the drug Nusinersen in clinical trials led by Richard Finkel, a physician at Nemours Children’s Hospital. This was the first time a drug improved patients’ motor skills and significantly extended their survival. Nusinersen was approved at the end of 2016, and more than 7,500 patients have benefitted from its effects. The K. J. Zülch Prize, with a value of 50,000 euros, will be awarded on 12 September, 2019 in Cologne.

In Germany, about 300 children are born every year with spinal muscular atrophy, a degenerative disorder of a type of nerve cells. Up until just a few years ago, the diagnosis was a death sentence for many newborns.

About half of the patients develop the severe type I form of the condition. These children develop the first symptoms of muscle weakness either in the uterus or during their first months of life. They never learn to sit or crawl and usually die of respiratory failure and related infections before their second birthday. Children with the intermediate type II form usually live longer and can sit independently, but are confined to a wheelchair for life and have a shortened life expectancy. In the milder type III and type IV forms, the onset of the condition does not occur until later in childhood or adulthood and allows those affected to live a broadly normal life, albeit with a decline or loss of ambulation.

All patients with spinal muscular atrophy have one genetic defect in common: they lack SMN1, the gene responsible for production of the SMN (survival of motor neurons) protein. This protein is required to prevent the progressive death of a specific type of nerve cells in the spinal cord and brain stem, cells which are responsible for transmitting signals from the brain to the body’s muscles. However, humans have an almost identical second version of the gene: the SMN2 gene. Unfortunately, a largely defective transcript is made from this gene, and only a small amount of functional protein is produced as a result. The more copies of the SMN2 gene a patient has, the more functional SMN protein can be produced by that backup gene, and the milder the effects of the condition. Various research approaches are therefore focused on increasing the protein production from the SMN2 gene.

Erroneous splicing

As a biochemist, Adrian Krainer has been researching for decades how genes are transcribed and translated into proteins, and how the underlying mechanisms can be influenced. During gene transcription into RNA, sequences containing information for the protein, called exons, must be separated from non-coding sections (introns) and joined together. This editing process is known as RNA splicing. However, a mutation in an exon of the SMN2 gene causes that exon to be omitted most of the time during RNA splicing, producing only a truncated protein, which rapidly degrades.

Adrian Krainer has been researching a type of molecule that can be used to correct the defective RNA splicing. The so-called antisense oligonucleotides, are short RNA-like segments which bind to specific sites on the transcript of a gene and influence how the information from the gene is converted into protein. In the case of defective SMN2 RNA splicing, Krainer found a short segment of 18 nucleotides that would aid production of the entire protein.

In collaboration with Ionis Pharmaceuticals, Krainer used mice that do not produce their own SMN protein, but instead have two copies of the human SMN2 gene, to test their antisense oligonucleotides, called Nusinersen. These mice develop severe spinal muscular atrophy and die within ten days of birth. However, when Krainer’s team administered Nusinersen before the onset of symptoms, the mice developed no muscle atrophy, and survived for over 250 days.

Clincal studies with Nusinersen

Following these promising results, Richard Finkel and colleagues investigated the effectiveness and potential side effects of Nusinersen in clinical trials. These trials also produced astonishing results. In a study of infants with the type I disorder, the original intention was to determine whether the survival of non-ventilated patients was extended by administering Nusinersen. However, it soon became clear that patients were also developing well and achieving motor milestones, as a result of Nusinersen treatment.

The results of an interim analysis of the study were so positive that it became ethically unreasonable to withhold Nusinersen from the placebo group. These infants were then enrolled into another study, in order for them to also benefit from the drug. Finkel realized that for the first time a drug significantly alleviates or reverses the reduction in patients’ movement and extends survival. As a result of the successful clinical trials, Nusinersen was approved as a drug in the US at the end of 2016, with approximately 7,500 patients worldwide being treated with it to date.

The Prize Winners

Adrian Krainer studied biochemistry at Columbia University and earned his doctorate in biochemistry and molecular biology from Harvard University. To continue his research career, he moved to Cold Spring Harbor Laboratory, where he first carried out postdoctoral research, and then obtained a professorship. He has been a full professor there since 1994 and St. Giles Foundation Professor since 2009.

After studying chemistry and medicine, Richard Finkel moved to Harvard Medical School where he specialized in paediatrics and neurology. He subsequently worked as a paediatrician and neurologist in hospitals in Denver and Philadelphia. He is currently Professor of Neurology at the University of Central Florida and Head of Neurology at Nemours Children’s Hospital in Orlando.

Prize Winners 2018: Autoimmunity in neurological diseases

Jerome Posner, Angela Vincent and Josep Dalmau have uncovered new diseases and have improved outcomes for neurological deficits

Cancer, infections and other still undescribed factors can trigger the body’s immune system. In some patients this results in an autoimmune attack against healthy tissue such as cells of the nervous system. This can lead to deficits such as memory loss, seizures, movement disorders, muscle weakness, and psychosis. The Gertrud Reemtsma Foundation has now paid tribute to Jerome Posner, Angela Vincent and Josep Dalmau for their research into how autoimmunity produces these neurological disorders that include paraneoplastic and non-paraneoplastic neurologic syndromes and the antibody-mediated autoimmune encephalitis syndromes. Their work has been pivotal in ensuring that many of these disorders are now recognised and patients promptly treated offering the best opportunity for neurologic improvement. In recognition of their outstanding achievements, the researchers have been awarded the Gertrud Reemtsma Foundation’s K. J. Zülch Prize worth 50,000 euro. The award ceremony will take place in Cologne, Germany on the 21th of September 2018.

Medical practitioners have long been aware that autoimmune brain diseases can occur in patients with cancer. The scientists have made crucial advances in research into these immune diseases by providing detailed clinical descriptions and through the development of simple diagnostic tests, allowed practitioners to quickly recognize, diagnose, and treat these patients. Their work has also provided insights into how cancers and other triggers such as viral infections initiate the autoimmune attack. This has opened new avenues to research into how to prevent and optimally treat these diseases. For some patients, recognition of the autoimmune neurologic symptoms leads to the detection of a previously undetected cancer, allowing early cancer treatment and an increased chance of cure.

These diseases were largely unknown to the public but gained attention when in 2011 a polar bear named Knut drowned in his pool at the Berlin Zoological Garden. An autopsy revealed that one of the antibody-mediated autoimmune encephalitis syndromes known as anti-NMDA receptor encephalitis caused his unexpected demise. Then in 2012, a patient with this same disease wrote a best-selling novel about her experience.

The American Jerome Posner is considered a pioneer in the field of research into these syndromes and their causes, having systematically described many of the paraneoplastic diseases for the first time and developing the first blood tests used to diagnose these disorders. His former colleague from Barcelona, Spain, Josep Dalmau is known for discovering several autoimmune encephalitis syndromes, developing diagnostic tests, and revealing the mechanisms whereby the autoantibodies are directly responsible for the brain dysfunction.

British-born Angela Vincent initially studied autoimmune diseases of the peripheral nervous system in which signal transmission between nerves and muscles are impaired. This led her to the then revolutionary insight that certain antibodies can also attack the central nervous system. She subsequently developed the diagnostic methods widely used in hospitals today.

The Prize Winners

For many years, Jerome Posner was Head of Neurooncology at the Memorial Sloan-Kettering Cancer Center in New York and Professor of Neurology and Neuroscience at Cornell University in New York. Following his medical studies in Barcelona, Josep Dalmau initially worked as a neurologist before continuing his scientific career in Jerome Posner’s laboratory. He currently holds professorships at the University of Pennsylvania and the University of Barcelona.

Angela Vincent, a medically-qualified neuroimmunologist, worked at University College in London with the late Ricardo Miledi, and the Royal Free Hospital with the late John Newsom-Davis. She spent the last 30 years at the University of Oxford where until recently she ran a national and international diagnostic antibody service and research group. She currently holds honorary positions in Oxford and London.

The Zülch Prize

The K. J. Zülch Prize 2018 will be awarded at 10 o’clock on the 21th of September 2018 in the Hansasaal (main hall) at Cologne’s historic City Hall. Following the laudations by Uwe Schlegel and Thomas Münte, Angela Vincent will talk about her research into autoimmune diseases of the peripheral and central nervous system. Following the laudation by Mathias Bähr, Josep Dalmau will talk about the discovery of anti-NMDA receptor encephalitis.