Nobel laureate Karl Deisseroth says light-based brain-computer interfaces will take a little time to build

By Inside BCI · October 7, 2026

Karl Deisseroth shares this year’s Nobel Prize in Physiology or Medicine for a way to make nerve cells switch on and off in response to light. Asked what the work means for neurotechnology devices, he said light could in principle do the job electricity now does in brain-computer interfaces, but that the application “probably will take a little time to build.” The technique is closer to patients elsewhere: in an eye injection for inherited blindness that faces an FDA decision in the first half of 2027, and in psychiatric drugs whose development drew on optogenetic laboratory studies.

What the prize recognised

The Nobel Assembly at Karolinska Institutet announced on 5 October that the prize goes to Deisseroth, of Stanford University and the Howard Hughes Medical Institute, Peter Hegemann of Humboldt University of Berlin and Georg Nagel of the University of Würzburg, for their discoveries concerning light-gated ion channels and optogenetics.

Hegemann and Nagel identified channelrhodopsin, a protein in the single-celled green alga Chlamydomonas that opens a channel through the cell membrane when light hits it. In August 2005 a Stanford team led by Deisseroth, with Nagel as a co-author, put the gene for the protein into cultured rat neurons and made them fire on cue with millisecond pulses of blue light. Researchers have since used the method to switch chosen groups of neurons on or off in living animals and to trace which cells drive memory, emotion and behaviour.

What Deisseroth said about brain-computer interfaces

Brain-computer interfaces are largely built on electricity, Deisseroth said: they record the brain’s electrical activity, and in some cases feed signals back in by stimulating it electrically. Light offers another way for that communication to happen, in principle, though he placed that potential application a bit further out.

Using light in the brain this way adds a step that electrical implants skip. Nerve cells in the brain do not respond to light on their own, so an optogenetic interface would pair a gene therapy that makes chosen cells light-sensitive with a light source to drive them.

Where optogenetics is closest to patients

The eye is where optogenetics has reached patients in clinical trials. On the day of the prize Deisseroth pointed to tests in blind people with retinitis pigmentosa, an inherited disease that destroys the retina’s light-sensing cells, in which the treatment has given back some sensitivity to light.

One company running such trials, Nanoscope Therapeutics of Dallas, has filed for US approval. In September the FDA accepted its application for MOGENRY (sonpiretigene isteparvovec) for adults with retinitis pigmentosa and severe vision loss. It is a one-time injection into the eye, given in a doctor’s office, that carries a light-sensitive gene into the retina’s surviving bipolar cells. The engineered light-sensitive protein responds to ordinary ambient light, so patients need no goggles, and the treatment is designed to work whichever gene caused the disease, so no genetic test is needed first. Nanoscope expects an FDA decision in the first half of 2027.

The application rests mainly on RESTORE, a small sham-controlled trial in patients with advanced retinitis pigmentosa, in which both doses improved visual acuity more than sham injection at 52 weeks, and on follow-up showing the gains held at three years. In RESTORE, no treatment-related serious adverse events were reported over two years; the most common eye effects, inflammation and raised eye pressure, were mild to moderate. Nanoscope puts the number of Americans with retinitis pigmentosa at more than 100,000, of whom more than 25,000 are legally blind.

Nanoscope said in September that it expects to start a Phase 2 trial in geographic atrophy in 2026. That is the advanced stage of dry age-related macular degeneration, which Science Corporation’s PRIMA implant treats with a wireless chip under the retina and glasses that project near-infrared light onto it. PRIMA went on sale in Europe in July.

Optogenetics as a drug-discovery tool

Deisseroth also said that trials built on what he called indirect optogenetics are moving from Phase 2 to Phase 3 in autism and schizophrenia. In this approach optogenetics stays in the laboratory: researchers use it to find the cells behind a symptom, then test which drugs act on those cells.

MapLight Therapeutics, the Nasdaq-listed company he co-founded in 2018 and advises as a member of its scientific advisory board, is one company developing drugs this way, with Phase 2 results in both conditions. Neither of its programmes has started Phase 3.

Its schizophrenia drug ML-007C-MA met the primary endpoint of the Phase 2 ZEPHYR trial in July at its twice-daily dose; the once-daily dose did not reach statistical significance, and MapLight’s shares fell sharply that day. MapLight plans to meet the FDA before starting a Phase 3 trial, ZEPHYR-2, and expects results in 2028.

Its autism drug ML-004 missed its primary endpoint, a measure of social communication, in the Phase 2 IRIS trial in June. A prespecified analysis found an improvement in irritability, which MapLight called clinically meaningful, among adolescents who started the trial with at least moderate irritability. MapLight intends to discuss a Phase 3 programme in autism irritability with the FDA, and in August said it would weigh partnerships or other funding for ML-004 while putting most of its resources behind ML-007C-MA. The company held $351.3 million in cash and investments at the end of June, before agreeing a $150 million private placement in August.

Not disclosed

Deisseroth gave no timeline or named project for light-based brain-computer interfaces. Nanoscope has not disclosed a price for MOGENRY. MapLight has not said when its meetings with the FDA will take place, or whether a partner will fund a Phase 3 trial of ML-004.

What to watch

Whether the FDA approves MOGENRY in the first half of 2027, which would bring an optogenetic therapy to the US market.

Whether Nanoscope starts its geographic atrophy trial, setting up a gene therapy alongside the PRIMA implant in the same disease.

Whether MapLight starts ZEPHYR-2, and whether ML-004 finds a partner.

Whether any brain-computer interface company takes an optogenetic programme into human trials.

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Cross-reference to prior InsideBCI coverage:

news Nobel-Prize optogenetics Karl-Deisseroth Peter-Hegemann Georg-Nagel channelrhodopsin Stanford Nanoscope-Therapeutics MOGENRY retinitis-pigmentosa gene-therapy MapLight-Therapeutics schizophrenia vision-restoration PRIMA