Defects and asymmetries in the visual pathway of non-human primates with natural strabismus and amblyopia.

Strabismus and amblyopia are common ophthalmologic developmental diseases caused by abnormal visual experiences. However, the underlying pathogenesis and visual defects are still not fully understood. Most studies have used experimental interference to establish disease-associated animal models, while ignoring the natural pathophysiological mechanisms. This study was designed to investigate whether natural strabismus and amblyopia are associated with abnormal neurological defects. We screened one natural strabismic monkey ( Macaca fascicularis) and one natural amblyopic monkey from hundreds of monkeys, and retrospectively analyzed one human strabismus case. Neuroimaging, behavioral, neurophysiological, neurostructural, and genovariation features were systematically evaluated using magnetic resonance imaging (MRI), behavioral tasks, flash visual evoked potentials (FVEP), electroretinogram (ERG), optical coherence tomography (OCT), and whole-genome sequencing (WGS), respectively. Results showed that the strabismic patient and natural strabismic and amblyopic monkeys exhibited similar abnormal asymmetries in brain structure, i.e., ipsilateral impaired right hemisphere. Visual behavior, visual function, retinal structure, and fundus of the monkeys were impaired. Aberrant asymmetry in binocular visual function and structure between the strabismic and amblyopic monkeys was closely related, with greater impairment of the left visual pathway. Several similar known mutant genes for strabismus and amblyopia were also identified. In conclusion, natural strabismus and amblyopia are accompanied by abnormal asymmetries of the visual system, especially visual neurophysiological and neurostructural defects. Our results suggest that future therapeutic and mechanistic studies should consider defects and asymmetries throughout the entire visual system.

[Mechanism of Bruch's Membrane in the Occurrence and Development of Myopia].

Myopia is a process of ocular wall remodeling along with axial elongation after emmetropia decompensation, but the causal relationship among the changes taking place in ocular fundus structures during this process is not clear. The choroid, which lies between the retina and the sclera, plays an important role in the transmission of information related to myopia. The role of choroid in myopia is a hot research topic at present. Findings from animal experiments showed that form deprivation-induced changes in choroidal thickness may be related to the vascular perfusion, but the triggering mechanism of choroidal perfusion changes during the process of myopia still needs to to be further explored. Bruch's membrane is an elastic membrane located in the front of the choroid with good contractile properties. In the process of myopia, regional changes of the synthesis or biomechanics of Bruch's membrane may have formed the earliest structural basis of changes in choroidal thickness and blood flow. Taking choroidal thickness as a starting point, this paper focuses on the role and mechanism of Bruch's membrane in the occurrence and development of myopia, which may further deepen our understanding of the mechanism of changes in choroidal thickness, and provide a theoretical basis for the development of new therapeutic targets for myopia.