Adaptive Neuroplasticity Following Central Visual Field Loss in Macular Degeneration

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ABSTRACT Macular degeneration (MD) is retinal disease that causes severe visual impairment in nearly 7 million people in the U.S. This disease causes the progressive deterioration of photoreceptors in the center of the retina, known as the macula, and renders patients unable to see in the center of the visual field. As a consequence, patients with MD must rely on peripheral vision, making even the simplest everyday tasks, such as reading or recognizing faces, much more difficult. Reliance on peripheral vision is extremely problematic, as it possesses substantially lower resolution compared to central vision. In fact, many patients never fully adapt to using peripheral vision effectively. Interestingly, however, some patients become particularly skilled at using their spared peripheral vision. Prior work suggests that this adaptation to using peripheral vision happens at a processing stage beyond the retina, specifically in visual cortex. There is debate in the literature about whether or not brain regions that formerly responded to central (lost) vision remap their function to respond to peripheral (spared) vision. We address a different form of plasticity here: remodeling of the brain regions which originally responded to peripheral (spared) vision so that they are more capable of taking on the functions of central vision. Our hypothesis is that peripherally-representing visual cortex builds new connections after experience, and this changes the structure and function of that region. Using neuroimaging (Magnetic Resonance Imaging) in human participants, we have generated preliminary evidence that suggests that some of these changes may exist in the form of alterations to brain structure (neurite density and cortical thickness) and brain function (functional connectivity). For example, we have observed that the parts of visual cortex that respond to peripheral vision have greater cortical thickness in MD patients compared to healthy controls, suggesting a possible compensatory mechanism that may be associated with enhanced use of peripheral vision. Additionally, we have observed that peripheral regions of early visual cortex in MD patients are more strongly functionally connected to later visual areas that selectively respond to specific types of visual stimuli, such as facial features and words/letters. We will test the hypothesis that better use of peripheral vision in MD is associated with enhanced functional connectivity and enhanced structure (neurite density and cortical thickness). More specifically, we predict that enhanced visual function in MD will be related to stronger functional connectivity between peripheral areas of primary visual cortex and later visual areas that respond preferentially to categories of stimuli (i.e.- faces, and words). Additionally, we predict that greater neurite density and cortical thickness in primary visual cortex will be related to behavioral performance on visual processing tasks. These findings will help provide insight towards improving therapeutic interventions for MD, as well as uncover knowledge about the adult brain’s potential for adaptation to changes in experience.