The prize winners founded the research field of optogenetics and significantly advanced it. Thanks to their research, it is possible today to activate or deactivate nerve and muscle cells with high temporal and spatial precision using light instead of electrodes. Ernst Bamberg, together with his colleagues Peter Hegemann and Georg Nagel, discovered the specific properties of the light-sensitive ion channels known as the channelrhodopsins in single-celled algae.

Karl Deisseroth recognized the enormous potential of channelrhodopsins for neuroscience early on. With Georg Nagel and Ernst Bamberg in 2005, he transferred channelrhodopsin-2 to the nerve cells of rat brains and was thereby able to trigger action potentials through optogenetics for the first time. Moreover, he was successful in activating channelrhodopsins in free-moving rats. To do this, he conducted light directly into the brain using glass fibre cables. In this way, he could investigate how nerve cells create behaviours such as movement, fear or social behaviour in different species and how the learning and memory processes occur.

Peter Hegemann had already begun research into how algae perceives light at the Max Planck Institute of Biochemistry in Martinsried back in 1985. In 2002 and 2003 at the University of Regensburg with Georg Nagel and Ernst Bamberg, he was able to demonstrate the extraordinary way that algae rhodopsins function: by transferring rhodopsin genes to egg cells of the clawed frog, they determined that the algae rhodopsins combine light receptors and ion channels in a single protein.

Georg Nagel has been researching the electrophysiological properties of algae rhodopsins since the early 1990s. From 1995 at the Max Planck Institute of Biophysics, he and Ernst Bamberg were successful in transferring various bacteriological rhodopsins to frogs’ eggs and human nerve cells, as well as in describing their electrophysiological properties.

Thomas Gasser studied the genetic makeup of such families and discovered different genes that can lead to the development of Parkinson’s disease and other mobility disorders, such as Myoklonus-Dystonia syndrome. For example, he identified the LRRK2 gene as the trigger of the most common inherited form of Parkinson’s disease so far.

Furthermore, his work has shown that genetic factors are also important for the sporadic form of Parkinson’s disease. These mutations are relatively prevalent in the general population, but every single one of them increases the risk for Parkinson only very little. However, in combination with each other and possibly with other environmental factors they develop their detrimental effects. These findings are the basis for developing treatments of Parkinson’s disease itself instead of merely easing its symptoms.

Gasser, who was born in Stuttgart in 1958, specialised in the genetics of neurological disorders at an early stage in his career. Following a research period in Boston, he worked at the university hospital of the LMU Munich for several years. He has been a Director of the Department of Neurology with focus on neurodegenerative diseases of the Hertie Institute for Clinical Brain Research and the University Hospital Tübingen since 2003.

Robert L. Nussbaum researches the genetic causes of Parkinson’s disease and Lowe syndrome. He was the first scientist to identify alpha-synuclein in 1997 as a gene in which mutations cause its carriers to develop Parkinson’s disease. This discovery paved the way for the research on other genetic causes of neurological disorders. It also emerged from the research that mutations of the alpha-synuclein gene can not only cause a rare inherited form of Parkinson’s, but that normal alpha-synuclein is also a central feature of all forms of the disease. Robert L. Nussbaum has recently shown that the vegetative nervous system in transgenic mice with a mutated form of the gene undergoes pathological changes before such changes arise in the brain, similar to what occurs in human Parkinson’s disease. His research has contributed significantly to a paradigm shift in how we think about Parkinson’s disease, from a “brain only” to a systemic disease.

The second focus of the research carried out by the 60-year-old doctor, who previously worked at the National Institutes of Health outside Washington, D.C.,  and at the University of Pennsylvania, is Lowe syndrome. This rare genetic condition is inherited via the X sex chromosome, and causes intellectual disability, seizures, cataracts and kidney damage. Most sufferers die at a young age. In the early 1990s, Robert L. Nussbaum identified the OCRL1 gene as the cause of this disease. The gene product, an enzyme involved in the metabolism of phospholipids, is active in the Golgi apparatus, the cell’s sorting and transport organelle, and at the cell surface. This enzyme plays a role in the transport of certain proteins from inside the cell to the cell surface, and back again. Its precise function and the reason why its function loss damages so many of the body’s organs remain unclear. Robert L. Nussbaum’s team developed test systems with which the disease can be diagnosed in the foetus and was the first laboratory to offer genetic testing and counselling to affected families.

Multiple sclerosis is one of the most common diseases of the nervous system. It is an autoimmune disease in which the immune system attacks the patient’s own body - in this case the layer of insulation that surrounds the projections of nerve cells. This layer, which is known as the myelin sheath, is slowly destroyed by inflammatory reactions. The immune system forms antibodies that damage the myelin. As a result, the affected neurons can only transmit signals to a limited extent or are prevented completely from doing so. This causes a wide variety of disturbances to the nervous system, ranging from vision and swallowing disorders to tiredness and paralysis.

Alastair Compston is considered one of the leading experts in the field of multiple sclerosis. He is Head of the Department of Clinical Neurosciences at the University of Cambridge in England. The London-born neurologist has been researching the causes and treatment of multiple sclerosis for over 30 years. He was the driving force behind the establishment of the International Multiple Sclerosis Genetics Consortium in 2001, a research association that aims to identify risk genes for the disease. Thanks to this large-scale genetic analysis, increasing numbers of gene mutations have now been identified that can increase or reduce susceptibility to multiple sclerosis.

Alastair Compston is also conducting research into the effect of a potential new active agent against the development of the disease, the antibody alemtuzumab. Certain immune cells, the T lymphocytes, migrate from the blood to the brain and cause inflammation. This process can be prevented using alemtuzumab. According to Compston, alemtuzumab can relieve the symptoms experienced by patients in the early stages of the disease. In patients with advanced multiple sclerosis, however, it is ineffective. This discovery shows that the progress of the disease is determined by different factors at different stages. The immune system dominates the course and development of the disease in the early stages, while neurodegenerative changes in the nervous system predominate in the later stages.