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A light switch for the living brain: optogenetics wins the 2026 medicine prize
On 5 October 2026, the Nobel Assembly at Karolinska Institutet awarded the 2026 Nobel Prize in Physiology or Medicine jointly to Karl Deisseroth, Peter Hegemann and Georg Nagel “for their discoveries concerning light-gated ion channels and optogenetics”. Deisseroth works at the Howard Hughes Medical Institute and Stanford University in the United States; Hegemann at Humboldt University of Berlin and Nagel at the University of Würzburg, both in Germany. The prize amount is 12 million Swedish kronor, to be shared equally between the laureates, with a prize share of one third each.
Optogenetics is a method, not a molecule and not a doctrine. According to the Nobel Committee, it makes it possible to show how nerve cells shape memories, feelings and behaviours in the living brain, and the laureates “have laid the foundation of a new era in neuroscience”. Per Svenningsson, chair of the Nobel Committee for Physiology or Medicine, said: “Optogenetics provides opportunities for mapping the brain in a way that we could once only dream of.”
The Committee’s popular background opens with a quotation from a letter that Virginia Woolf wrote to a friend in 1932: “My own brain is to me the most unaccountable of machinery — always buzzing, humming, soaring, roaring, diving, and then buried in mud.” Researchers, it explains, had in the twentieth century identified which regions of the brain govern various functions, but the methods were relatively blunt and could not prove that a specific type of nerve cell directly caused a certain feeling or behaviour. The image of the brain was “like a blurry photograph, missing many details”. One of those who dreamed of a more precise tool was Francis Crick (Nobel Prize 1962), who concluded that light would probably be ideal for activating individual nerve cells, since the signals in nerve cells are extremely rapid.
The story starts with an alga. In the early 1990s Peter Hegemann, then at the Max Planck Institute for Biochemistry in Martinsried, asked how the single-celled alga Chlamydomonas can react so rapidly to light. It senses light with an eyespot, and Hegemann measured an electrical impulse just half a millisecond after light reached it. He formulated the hypothesis that a single protein complex both captured light and acted as an ion channel, a proposal that was met with scepticism. Around the turn of the millennium, after years of setbacks, his group found two candidate genes in the alga’s DNA, and Hegemann contacted Georg Nagel, then at the Max Planck Institute for Biophysics in Frankfurt. Nagel injected copies of the genes into frog egg cells, and the newly produced proteins turned out to be ion channels that opened when exposed to light. They were named channelrhodopsin-1 and channelrhodopsin-2. Hegemann and Nagel also introduced the gene for channelrhodopsin-2 into embryonic human kidney cells and kidney cells from hamsters, and the cells became light sensitive. They published the results in 2003.
After this, in the Committee’s words, a young scientist at Stanford University took the baton. Deisseroth had trained in medicine, spent part of his training at a psychiatric clinic, and, in parallel with his medical studies, gained a PhD in neuroscience. When his own research group was searching for a protein that could trigger electrical impulses in nerve cells, he heard of channelrhodopsin-2 and wrote to Nagel to ask for the DNA. He introduced it into rat nerve cells cultured in petri dishes; when the cells were exposed to blue light, the light provoked a nerve signal that could be propagated to other nerve cells. The group published the discovery in 2005. In 2006 the new method was given the name optogenetics, and a year later Deisseroth’s group introduced the gene into a specific nerve cell type in the motor cortex of living mice, fed a thin optic fibre through a small hole in the skull and used light to control the movement of the animals’ whiskers.
The Committee points to further early milestones. In 2007 Deisseroth and colleagues also woke sleeping mice by shining light on a type of nerve cell suspected of controlling wakefulness. In 2012, together with Susumu Tonegawa, he activated an engram, the pattern of neural pathways formed when a memory is created; mice whose fear-memory cells were reactivated showed signs of fear despite not being in danger. According to the Committee, researchers can now “bring memories to life, create feelings, drive behaviours” and study the types of neurons involved in psychiatric and neurological disorders. They have also identified neural circuits governing pain, social behaviour, thirst, food consumption, reward and attention.
The Committee is careful about medicine. The method, it says, has provided greater understanding of disorders such as depression, anxiety, schizophrenia, Alzheimer’s disease and Parkinson’s disease, and researchers have taken “the first steps” towards using optogenetics as a treatment. In ongoing clinical trials they attempt to restore vision in people who have become blind due to retinitis pigmentosa, a disease that destroys the eye’s rods and cones. When a channelrhodopsin-like protein was inserted into the retina of a blind person, the person regained some vision and, using special glasses emitting light, was able to discern and grasp objects on a table. The Guardian reports the same trial as partially restoring the sight of a man blinded by the condition. There are also hopes that optogenetics could improve cochlear implants.
For a readership outside the sciences, the laureates’ story carries a modest moral. The work began as curiosity about how an alga finds light, and it passed through frog eggs, kidney cells and rat neurons before it reached the living mouse brain, over roughly two decades from Hegemann’s first hypothesis. The prize honours the method rather than any cure, and the Committee is explicit that clinical uses are still at an early stage.
Karl Deisseroth. Photo: Christopher Michel / Wikimedia Commons, CC BY-SA 4.0.
