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Early reports documented degeneration of retinal ganglion cells and their axonal projections. Our data suggest that the brain and retina follow a similar trajectory during AD progression, probably due to their common embryonic origin and anatomical proximity. However, the retina is the only CNS organ feasible for direct, repeated, and non-invasive ophthalmic examination with ultra-high spatial resolution and sensitivity.
Neurovascular unit integrity is key to maintaining normal CNS function and cerebral vascular abnormalities are increasingly recognized as early and pivotal factors driving cognitive impairment in AD. Likewise, retinal vascular abnormalities such as changes in vessel density and fractal dimensions, blood flow, foveal avascular zone, curvature tortuosity, and arteriole-to-venule ratio were described in AD patients including early-stage cases.
A rapidly growing number of reports have suggested that cerebral and retinal vasculopathy are tightly associated with cognitive deficits in AD patients and animal models. Other studies utilizing optical coherence tomography OCT , retinal amyloid-fluorescence imaging and retinal hyperspectral imaging have made significant progress in visualizing and quantifying AD pathology through the retina. With new advances in OCT angiography, OCT leakage, scanning laser microscopy, fluorescein angiography and adaptive optics imaging, future studies focusing on retinal vascular AD pathologies could transform non-invasive pre-clinical AD diagnosis and monitoring.
AD patients progressively develop irreversible cognitive loss due to neurodegeneration in the brain and other direct or indirect factors such as accumulation of toxic molecules, neuroinflammation, and vascular damage. Our group identified these hallmarks in the retina of postmortem and living AD and mild cognitively impaired MCI patients Koronyo-Hamaoui et al. Vascular pathology in AD is an expanding subject and a growing number of studies show that vascular-related damage in the brain and retina can predict cognitive decline Vidal and Mavet, ; Baker et al.
