ABSTRACT
Purpose We investigated the impact of age-related macular degeneration (AMD) on visual acuity and the visual white matter.
Methods We combined an adaptive cortical atlas and diffusion-weighted magnetic resonance imaging (dMRI) and tractography to separate optic radiation (OR) projections to different retinal eccentricities in human primary visual cortex. We exploited the known anatomical organization of the OR and clinically relevant data to segment the OR into three primary components projecting to fovea, mid- and far-periphery. We measured white matter tissue properties – (fractional anisotropy, linearity, planarity, sphericity) along the aforementioned three components of the optic radiation to compare AMD patients and controls.
Results We found differences in white matter properties specific to OR white matter fascicles projecting to primary visual cortex locations corresponding to the location of retinal damage (fovea). Additionally, we show that the magnitude of white matter properties in AMD patients’ correlates with visual acuity. In sum, we demonstrate a specific relation between visual loss, anatomical location of retinal damage and white matter damage in AMD patients. Importantly, we demonstrate that these changes are so profound that can be detected using magnetic resonance imaging data with clinical resolution. The conserved mapping between retinal and white matter damage suggests that retinal neurodegeneration might be a primary cause of white matter degeneration in AMD patients.
Conclusions The results highlight the impact of eye disease on brain tissue, a process that may become an important target to monitor during the course of treatment.
Author Contributions
Designed the study: SO HT TN YM. Performed the experiments: SY SO HH MT AM YM. Analyzed the data: SY SO HH FP. Institutional support: KM. Wrote the paper: SY SO HH FP.
Acknowledgements
We thank Brian A. Wandell, Sophia Vinci-Booher, Brent McPherson and Bradley Caron for comments on an early version of the manuscript. Takaaki Hayashi for clinical evaluation of the patients. Ikuya Murakami for institutional support. YS is supported by JSPS Grant-in-Aid for Young Scientists (B) 80570332. SO is supported by JSPS Grant-in-Aid for Young Scientists (B) 17K18131. HH is supported by JSPS Grant-in-Aid for Young Scientists (B) 26870605. YM is supported by The Jikei University Research Fund. F.P. is supported by NSF IIS-1636893, NSF BCS-1734853, NIH NIMH ULTTR001108, a Microsoft Research Award and the Indiana University Areas of Emergent Research initiative “Learning: Brains, Machines, Children,” and Pervasive Technology Institute.
Footnotes
Disclosure of potential conflicts of interest. Authors declare no conflict.
Research involving Human Participants and/or Animals. Research was approved by the ethical committees of the Jikei University School of Medicine, Tamagawa University, and Atsugi City Hospital.
Informed consent. All participants provided written informed consent to participate in the project.