Visual evoked potentials (VEPs) are the electrical signals the brain generates in response to light, and they have long been a fixture of clinical neurology. But in preclinical research, they are earning a second reputation: as sensitive, quantitative measures capable of tracking disease progression and treatment response in the central nervous system with a precision that few other non-invasive tools can match. Three recent studies illustrate just how far that potential extends, from models of demyelinating disease to newborn monkeys whose brain development was disrupted by a mosquito-borne virus.
Proving That Remyelination Is Actually Happening
One of the persistent challenges in developing therapies for demyelinating diseases like multiple sclerosis is demonstrating, objectively and over time, that a treatment is doing what it is supposed to do. Tissue sampling requires sacrificing the animal. MRI has resolution limits. VEPs offer something different: a functional readout of white matter integrity that can be measured repeatedly in the same animal without any intervention.
A 2019 study in PNAS (Heidari et al.) established the foundation clearly. Using animal models of demyelination and remyelination, the investigators showed that flash VEPs, specifically the timing of the brain’s major electrical response, track myelin status with remarkable fidelity. As the protective myelin sheath around nerve fibers breaks down, conduction slows and the VEP response is delayed; as remyelination proceeds, timing recovers toward baseline. The match between the electrical measurements and what was observed in tissue samples was strong enough to position VEPs as a reliable functional indicator of myelin repair.
That foundation was then put to work in a 2025 study in Experimental Neurology (Duncan et al.), which examined the effects of a compound designed to mimic thyroid hormone signaling on remyelination and functional recovery. Thyroid hormone is known to support the repair of the myelin sheath, but demonstrating that a drug candidate produces real functional benefit (not just tissue-level changes) requires a measure that captures how the nervous system is actually working. VEPs provided exactly that. Animals treated with the compound showed measurable recovery in response timing that paralleled remyelination in tissue, and that recovery translated into improved functional outcomes. The electrical data were not merely confirmatory; they were central to the argument that the drug was producing meaningful neural repair.
Together, these two studies make a compelling case that VEPs are not just a convenient stand-in measure but a genuine endpoint in their own right: one whose meaning is grounded in the underlying biology, sensitive to the changes of interest, and applicable across species. That last point matters. VEP timing is measured clinically in MS patients; establishing that it tracks myelin status in preclinical models in the same way creates a direct bridge between animal data and human trial endpoints, one that is difficult to build with tissue sampling or imaging alone.
A Primate Window Into Prenatal Zika
The value of VEPs extends well beyond demyelination. A 2026 study in Nature Communications (Ausderau et al.) used visual brain recordings as part of a comprehensive assessment of how Zika virus infection during pregnancy affects brain development in infant macaques.
The Zika epidemic made clear that infection before birth could produce severe neurological outcomes, with microcephaly being the most visible. But the range of effects in infants born without obvious structural damage remained poorly understood, partly because the tools for detecting subtle functional disruption in very young children are limited. Nonhuman primates offer a model system with close developmental parallels to humans, and electrical brain measurements offer a way to probe brain function without requiring the kind of behavioral cooperation that infants cannot provide.
The study found that Zika exposure before birth disrupted both social-emotional development and visual brain function in infant macaques, with VEP-based measures revealing abnormalities in visual processing that were not apparent from brain scans alone. This is precisely the kind of finding that preclinical brain recording is positioned to deliver: a sensitive functional signal that connects to a clinically meaningful question. In this case, that question is what happens to the developing brain when a fetus is exposed to a virus capable of causing birth defects.
The Broader Point
What connects these three studies is not just methodology but scientific logic. VEPs work as preclinical measures because their meaning is specific: a delayed response tells you something concrete about myelin, and an altered response pattern tells you something concrete about how visual information is being processed in the brain. They also have direct equivalents in clinical practice. That connection between the lab and the clinic, running in both directions from bench to bedside and back, is what makes them worth treating as endpoints in their own right, not simply as supplements to tissue analysis or imaging.
As the range of conditions in which VEPs are being applied continues to expand, from classic demyelinating disease to virus-induced developmental injury, the case for building them into preclinical study designs from the outset becomes increasingly difficult to ignore.
References
Heidari M, et al. Evoked potentials as a biomarker of remyelination. PNAS. 2019;116(52):27074–27083. https://www.pnas.org/doi/10.1073/pnas.1906358116
Duncan ID, et al. Promotion of remyelination by a thyromimetic drug leading to functional recovery. Exp Neurol. 2025;389:115227. https://www.sciencedirect.com/science/article/abs/pii/S0014488625000913
Ausderau KK, et al. Prenatal Zika virus exposure disrupts social-emotional development and cortical visual function in infant macaques. Nat Commun. 2026;17:1803. https://www.nature.com/articles/s41467-026-68517-x