What This Year's Nobel Tool Has Done in MS So Far

On 5 October 2026 the Nobel Assembly at Karolinska Institutet gave the Prize in Physiology or Medicine to Karl Deisseroth, Peter Hegemann and Georg Nagel for the discoveries that led to optogenetics, the ability to switch individual nerve cells on or off in a living brain using light and genetics. The timing makes this review worth reading now. AbouShawareb and colleagues set out to answer a narrower question than the prize does: what has the technique produced in multiple sclerosis (MS) specifically, and how close is any of it to a patient? They searched PubMed, Scopus and Web of Science for work published between 2022 and 2024 using the terms multiple sclerosis, MS, optogenetics, myelination and Schwann cells, and included experimental optogenetics trials in experimental autoimmune encephalomyelitis and in neurons. The search returned 58 articles related to the topic, of which 9 were included. What follows is a narrative review of those 9, and almost all of the evidence in it comes from animals and cultured cells.

What the Technique Needs to Work
Making a cell answer to light requires three things: light-activated proteins, light itself, and a way to deliver the first. The proteins are microbial opsins, delivered to neurons either by viral carriers such as lentivirus or adeno-associated virus carrying the opsin gene, or non-virally. Light reaches them through an optic fibre, which can get to deeper brain structures, with a light-emitting diode the most effective source. One tool used repeatedly in the work reviewed here is channelrhodopsin, which is precisely where the Nobel connects to the MS literature: the channelrhodopsins came out of Hegemann and Nagel's work on how algae respond to light, and Deisseroth's contribution was getting them into neurons so that a light pulse becomes a firing command. Outside MS the technique already runs in several fields, including visual restoration in ophthalmology by altering surviving retinal neurons, arrhythmia treatment and cardiac resynchronization under precise low-energy optical control, cancer research combined with gene-editing systems, and neuropsychiatry for the circuits of depression and pain.

Using Light to Ask a Question About Cause
The first MS use in the review is not therapeutic at all, but investigative. Heterogeneous nuclear ribonucleoprotein A1 has a role in RNA processing and cellular stress responses, and mutations in it, particularly P275S and F281L, have been identified as contributors to neurodegenerative processes in MS. These mutations lead to cytoplasmic mislocalization of the protein, which alters the kinetics of its cluster formation and increases the formation of stress granules. Optogenetic systems using blue light stimulation can speed that granule formation up, which converts a slow and variable cellular process into something a researcher can trigger on demand and watch unfold. The review's reading is that this mislocalization and the cellular stress responses that follow may worsen neurodegeneration and underlie the cognitive impairment seen in people with MS.

A Drug Released by Near-Infrared Light
Interferon beta was the first disease-modifying therapy for MS, cutting relapse rates and delaying the onset of disability. Once it binds its receptors it raises anti-inflammatory cytokines including IL-4, IL-5, IL-10, IL-13 and transforming growth factor β, and lowers proinflammatory ones including IL-17 and IFN-γ. Its weakness is injection frequency and the adherence problem that follows, and one trial addressed that with a wireless bioelectronic cell-based implant. The device uses immortalized human mesenchymal stem cells, chosen for their immunomodulatory properties, genetically engineered to express a bacteriophytochrome diguanylate cyclase. Near-infrared light activates that enzyme, which produces cyclic di-guanosine monophosphate, which in turn activates the stimulator of interferon genes pathway. That leads to phosphorylation of interferon regulatory factor 3, which moves to the nucleus and drives expression of the interferon beta gene, releasing the protein into surrounding tissue. Being wireless, the device avoids the invasive fibre optic implants the traditional approach needs, with their risks of infection and tissue damage, while allowing control over the timing and amount released. Tested in an EAE mouse model, these Optoferon cell devices significantly prevented acute demyelination.

Remyelination, Attempted Through Two Different Cell Types
Oligodendrocytes are the main remyelinating cells in the CNS, and one experiment applied optogenetic-based electric stimuli to the demyelinated corpus callosum of mice using 30-second light pulse trains at 20 Hz repeated every 4.5 minutes, a protocol designed to reach demyelinated axons without disturbing wider circuit function. Repeated stimuli enhanced neuronal activity and promoted differentiation of oligodendrocyte precursor cells into mature oligodendrocytes, with ultrastructural improvements and increased functional recovery in the affected axons. Schwann cells gave a parallel result in the peripheral nervous system. Optogenetic stimulation raised calcium in the stimulated cells, drawn from inositol trisphosphate-sensitive stores and brought inward through T-type voltage-gated calcium channels, and that calcium signalling drove both proliferation, evidenced by higher counts of bromodeoxyuridine-positive cells, and differentiation through expression of EGR2 and myelin basic protein. Motor neurons transfected with a channelrhodopsin gene and given 20 Hz pulses for an hour produced more Schwann cells expressing myelin basic protein, and the stimulated neurons carried a thicker, more compact myelin sheath with thickness approaching in vivo estimates. The g-ratio, the ratio of the axon's inner diameter to the myelinated fibre's total outer diameter, approached its theoretical optimum for nerve conduction under Schwann cell stimulation. A comparative study found that stimulating Schwann cells produced higher rates of myelination in the peripheral nervous system than stimulating neurons, which the review suggests may shift future attention toward Schwann cells.

The Cognitive Argument
Cognitive impairment is common in MS and affects quality of life, and the review treats optogenetics as a possible route to it by selectively activating the neural circuits involved in learning and memory. The supporting evidence is that optogenetic activation can promote neuroplasticity, and that stimulating the prefrontal cortex enhanced working memory performance in animal models, which the authors extend as a suggestion that similar approaches could help people with MS who have cognitive deficits. They then tie this back to the first strand: combining optogenetics with therapies aimed at correcting impaired hnRNP A1 function could, in their reading, produce interventions that mitigate neurodegeneration and improve cognitive resilience.

What the Review Says Stands in the Way
The obstacles are set out without softening. MS is a complex disease with many patterns, so developing one technology that treats all types with the same efficacy will be difficult. The need for genetic engineering to introduce opsins raises ethical questions, especially about human use, alongside the possibility of an immune response to microbial opsins and the open question of whether introducing these genes leads to lasting genetic change. Patterned neural activity can alter gene transcription and induce epigenetic changes, and tumour formation is among the risks that follow. Using the tools on the brain carries risk of CNS infection and tissue damage. The complexity of neural circuits calls for more refined targeting and control methods to ensure that an intervention is specific and effective. The authors close by saying it is crucial to conduct more research and clinical trials on the efficacy of optogenetics in MS and to work on minimizing potential adverse effects. Their own scope sets the frame for all of it: nine papers, published between 2022 and 2024, drawn overwhelmingly from animal models and cell culture.

Disclaimer: This blog post is based on the cited review and is intended for informational purposes only. It is not intended to provide medical advice. Please consult with a healthcare professional for any health concerns.

Reference:
AbouShawareb, H., Attiya, B., Alnajjar, A. Z., Meshref, M., & Obeidat, A. Z. (2026). The emerging role of optogenetics in multiple sclerosis research. International Journal of MS Care, 28(3), 180–185. https://doi.org/10.7224/1537-2073.2025-019
The 2026 Nobel Prize in Physiology or Medicine was announced on 5 October 2026: https://www.nobelprize.org/prizes/medicine/2026/summary/