The 2026 Nobel Prize in Physiology or Medicine recognizes optogenetics, a method for switching individual neurons on and off with light that has already restored a blind person's ability to locate objects on a table
The 2026 Nobel Prize in Physiology or Medicine recognizes optogenetics, a method for switching individual neurons on and off with light that has already restored a blind person's ability to locate objects on a table
On 5 October 2026, the Nobel Assembly at Karolinska Institutet awarded the prize in Physiology or Medicine to Karl Deisseroth, Peter Hegemann and Georg Nagel “for discoveries concerning light-sensitive ion channels and optogenetics.” Hegemann and Nagel discovered the mechanism in a single-celled alga; Deisseroth brought it to animal brains and clinical practice.
In 1979, Francis Crick, who received the Nobel Prize in 1962 for discovering the structure of DNA, described how to establish that a particular type of neuron causes a behavior: switch those neurons on and off at the speed at which they normally fire. He called his idea “rather far-fetched,” since no suitable tool existed at the time.
Researchers had already tried activating neurons with lasers and chemical switches, but lasers damaged cells, while chemical switches were too slow. In the early 1990s, Peter Hegemann was recording the electrical response of the alga Chlamydomonas reinhardtii to a flash of light when he detected a pulse after just half a millisecond. This was faster than the chemical cascade then known to underlie vision could explain. The light-sensitive proteins known at the time were slow pumps that moved ions against a gradient. Hegemann proposed that a single protein could serve as both a photoreceptor and a fast ion channel. Georg Nagel introduced candidate genes from the alga into frog egg cells: the channel opened 0,2 milliseconds after a flash. The proteins were named channelrhodopsin-1 and -2 (2002–2003), confirming the hypothesis.
During his psychiatry residency, Karl Deisseroth saw the suffering of patients with depression, autism and schizophrenia. He concluded that understanding these conditions required an understanding of the brain's neural circuits. In 2005, he introduced the channelrhodopsin-2 gene into rat neurons: a flash of blue light triggered a single nerve impulse with millisecond precision. A year later, he and his colleagues proposed the term “optogenetics.” In 2007, light delivered through an optical fiber made a freely moving mouse twitch its whiskers, and activating neurons involved in wakefulness that expressed the gene woke sleeping mice. This provided the very evidence Crick had considered unattainable: activity in a specific type of neuron causally produces a behavior.
In 2006, introducing the channelrhodopsin-2 gene into the retinas of mice with retinitis pigmentosa, a disease in which the light-sensitive rods and cones die, restored light sensitivity in the surviving retinal cells that relay signals onward. In 2021, José-Alain Sahel and Botond Roska reported in Nature Medicine the case of a blind patient with the same diagnosis. A gene encoding the protein Chrimson was introduced into his surviving cells, and he was given goggles equipped with light-emitting diodes. The patient learned to distinguish and pick up objects on a table, and EEG recordings confirmed activity in his visual cortex.
“Optogenetics offers possibilities for mapping the brain in ways we could previously only dream of,” said Per Svenningsson, chair of the Nobel Committee for Physiology or Medicine.
The same tool can also control memory. In 2012, Deisseroth and Nobel laureate Susumu Tonegawa's group used a gene encoding a light-sensitive protein to label neurons that were active when a mouse experienced fear. A subsequent flash of light in a safe setting elicited the same fear response, showing that a specific memory had been activated.
The path from an alga's response to light to a human therapy took twenty years, and development continues: MCO-010 for retinitis pigmentosa is being prepared for FDA approval.