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Updated: Jun 2, 2026

Inducement and Evaluation of a Murine Model of Experimental Myopia
Published on: January 22, 2019
Neuro-ophthalmic review on pediatric myopia: Advancing from refraction to a brain-centric model of axial growth
Matteo Capobianco1,2, Simonetta Gaia Nicolosi2, Edoardo Dammino2
1Eye Clinic, Policlinico G. Rodolico, University of Catania, Catania 95121, Italy.
Abstract:
Pediatric myopia is conventionally characterized as a refractive anomaly influenced by optical defocus and environmental factors. Emerging evidence suggests that axial elongation during childhood may be usefully reframed through a neuro-ophthalmic perspective, integrating retinal signaling, visual cortex maturation, and neuroplasticity. This minireview examines myopia within an eye-brain axis framework, emphasizing the roles of retinal neurotransmitters, dopaminergic pathways, and visual processing networks in regulating eye growth. Here, "brain-centric" denotes a clinically integrative model in which neurodevelopmental state and brain-governed behaviors (e.g., sleep/circadian timing, viewing habits, outdoor exposure) shape the visual inputs that engage established intraocular growth pathways, rather than implying that post-retinal processing is required for emmetropization. Advances in high-resolution imaging, electrophysiology, and functional neuroimaging have reported structural and functional differences in the retina and central visual pathways that may be detectable early during myopia development; however, evidence that such alterations consistently precede refractive error remains limited, and causal direction is not fully established. We examine how early visual experiences, sleep, digital viewing behaviors, and neurodevelopmental factors may influence these pathways in children. Reconceptualizing pediatric myopia within an eye-brain axis framework may support targeted prevention, individualized monitoring, and treatment selection, as well as hypothesis-driven predictive work to identify higher-risk trajectories, while avoiding causal overinterpretation when evidence remains primarily associative.
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