Nihon ryōiki is known as the earliest extant Buddhist anecdotal collection in Japan. Very little is known about its compiler, a monk named Kyōkai who belonged to the lower aristocracy and was active in the provinces rather than at the central court. Nihon ryōiki was compiled to keep a record of the miraculous events occurred in Japan. Like the tales documented in Buddhist sutras and Chinese anecdotal collections, Kyōkai insisted that similar events had happened in Japan in different ages and areas. Evidence of such miraculous events indicated, in Kyōkai’s view, that Japan, like India and China, was a land that deserved the Buddha’s salvation. Nihon ryōiki makes the case that the reason miraculous events occurred equally in Japan is the existence of Japanese sages of great virtue who were not inferior to Chinese sages. Although the reliability of the historical accounts in Nihon ryōiki is somewhat questionable, I am not interested in whether the Nihon ryōiki stories have any basis in reality, but rather in what has been changed and why the changes have been made. Stories that are adaptations from sutras or Chinese sources have been modified and adapted to become miraculous events that supposedly occurred in Japan. In the first chapter, I discuss how Kyōkai establishes a Japanese lineage of sagehood as evidence of Japan being a sacred land. In the second chapter, I focus on Prince Nagaya, who is depicted as a sinner who receives the penalty of death because he is unable to identify a “hidden sage”. In the third chapter, I examine the historical context of the Chinese monk Jianzhen’s arrival at Japan and introduce how Tiantai teachings were promoted by Jianzhen’s disciples, how a tale that asserted Prince Shōtoku was a reincarnation of monk Huisi spread. I also make a comparison between the Nihon ryōiki and a Chinese anecdotal collection titled Min bao ji to examine how Chinese influences are vernacularized and changed. Nihon ryōiki adopts a deliberate and consistent policy of vernacularizing its Chinese sources by changing key details in the stories and thereby adapting them to a Japanese context.

This dissertation seeks to clarify links between non-invasive radiological and optical biomarkers, neuropathology and neurodegeneration within axon tracts during neurodegenerative disease, with focus on Alzheimer's Disease (AD). Data contained in these studies were gathered from a variety of different model systems with different modes of neurodegeneration relevant to human clinical findings. Our studies utilized the visual system to model the axonal degeneration process and evaluate biomarkers of axon tract injury. First, a comprehensive analysis of visual system white matter integrity was performed in AD, MCI and control patients, using diffusion tensor images (DTIs) drawn from the Alzheimer's Disease Neuroimaging Initiative. Our findings establish the visual system as a white matter pathway affected during AD. Next, we used a retinal ischemia model to characterize spatiotemporal patterns of axonal degeneration in the visual system by DTI in Wallerian Degeneration Slow mice. Our results reveal an ability to identify propagating anterograde degeneration along the optic nerve and tract. Next, we used a Experimental Autoimmune Encephalomyelitis model to simulate retrograde axonal degeneration in the visual system and characterize the longitudinal relationship between DTI-measured axon loss and optical coherence tomography measured retinal thinning. Our data clarify the relationship between the biomarkers, and establish the correlation between each and magnitudes of axon loss. Next, we evaluated whether axonal transport function, a key putative factor in AD-related axonal degeneration could be related to DTI properties in the p301L tau transgenic model using Manganese-enhanced MRI. Our data expose a novel connection between restricted diffusion in the ON and compromised axonal transport function. Lastly, we tested whether retrograde axonal degeneration could be triggered by Aβ-induced tau pathology. Our results reveal a temporal pattern of damage that appears to emanate from the presyanpse toward cell bodies, and result in loss of white matter integrity in a manner similar to what is observed in humans during AD. Additionally, our experiments reveal the critical role of initial Aβ-induced tau phosphorylation, and imply that blocking this step by microtubule-stabilizing compounds may prevent downstream axon and cell loss. This process may be integral to understand the widespread white matter damage observed in Alzheimer's Disease.