Optogenetic gene therapy was safe in 10 blind people with advanced retinitis pigmentosa, six of whom gained clinically meaningful light sensitivity. The gains were measured within each patient in a small dose-escalation study, so the result supports safety and shows the approach works in people while sharp vision stays years away.
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Peter Hegemann, Georg Nagel and Karl Deisseroth won this year's medicine Nobel for optogenetics, which uses light to switch on chosen neurons. With it, researchers can switch on one circuit and see whether a behavior follows, a direct test of cause.
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Karl Deisseroth, Georg Nagel and Peter Hegemann won the 2026 medicine Nobel for optogenetics, the control of cells with light and genetics. It goes to a laboratory method, unlike the discoveries and treatments Scientific American cites from the prize's 125-year record.
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Optogenetic gene therapy restored some vision to people blinded by retinitis pigmentosa in a small NEJM trial. Seven of 10 participants improved in light sensitivity, Science News reported, though the goggle-aided sight let none of them read words or see faces.
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Optogenetics, the use of light to control neurons millisecond by millisecond, won its developers the 2026 Nobel Prize in physiology or medicine. A neuroscientist's account places it third, after tools for seeing and measuring the brain, and treats the therapies it may enable as projections.
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Indian Institute of Science biologists switched on the division enzyme Aurora A with blue light, bypassing its scaffold Cep192, in living human cells. The result backs the idea that clustering is what activates the kinase, and it gives researchers a reversible, light-driven way to test what spindles need from the centrosome.
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Researchers at Texas A&M built four blue-light switches that let a lab watch, redirect and sever the microtubule tracks inside a living cell, reversibly. Published in Cell Reports Methods, the set is built to test whether transport failures help drive cancer and dementia.
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A Hebrew University team traced cocaine's compulsive licking in mice to the orofacial action-selection circuit of the ventrolateral striatum, then turned the behavior off and on by moving the region's two competing pathways.
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Recordings from 422 neurons in two mouse visual areas, and a network model fitted to them, indicate that reciprocal loops sustain activity the two areas share and let mismatched activity decay within a fraction of a second.
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Salk researchers recorded and then manipulated the amygdalostriatal transition zone in freely moving mice, and report in Neuron that dopamine-expressing neurons there are needed to mount a fear response.
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DTU's mAxialtrode packs a light-guiding core and eight liquid channels into a fiber thinner than half a millimetre. It worked in mice, and its developers say routine clinical use needs much more testing and regulatory approval.
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Researchers report FenixS, a 17-kDa monomeric biliverdin-binding photoreceptor, and Ash1, a 6-kDa binder whose affinity for it rises more than 1,200-fold under 700-nm light in mammalian cells with no added cofactor.
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Steve Ramirez's 2013 mouse result turned on an injection that missed its target, and the book he has written since names PTSD and dementia as goals, which puts the question of who authorizes an edit ahead of the evidence.
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