Abstract Body

There is increasing agreement that anatomical changes in the retina may provide an opportunity for identifying and quantifying central nervous system (CNS) amyloid levels. Additionally, when compared with healthy age-matched controls, patients with AD have reduced numbers of ganglion cell axons, and they are three times more likely to have increased optic nerve cup-to-disc ratio, a potential consequence of ganglion cell and nerve fiber loss. Further, peripapillary retinal nerve fiber layer (RNFL) thickness appears to be reduced (suggestive of optic atrophy) in patients with mild cognitive impairment (MCI) and mild-to-moderate AD when compared with age-matched controls. We have recently shown that individuals with likely preclinical AD have corresponding thinning of the macular RNFL. Finally, several groups have reported decreased retinal vascular bed complexity, blood flow and oxygen consumption in MCI and AD, in comparison to matched control participants. A number of these retinal changes are also the result of effects of normal aging, and there is generally a paucity of data describing longitudinal changes over time within the same subjects, with respect to the retinal layers, the retinal microvasculature, and aggregation of inclusion bodies that may contain fibrillar beta-amyloid (Aβ) from the earliest, preclinical stage of AD. The purpose of this presentation will be to present an update on what we can conclude from available literature, new trends and developments in this field, and what questions remain open and uncertain, with respect to the development of retinal biomarkers of AD.