Abstract
Alzheimer's Disease (AD) is a devastating neurodegenerative disorder of the brain, clinically characterised by cognitive deficits that gradually worsen over time. There is, at present, no established cure, or disease-modifying treatments for AD. As life expectancy increases globally, the number of individuals suffering from the disease is projected to increase substantially. Cumulative evidence indicates that AD neuropathological process is initiated several years, if not decades, before clinical signs are evident in patients, and diagnosis made. While several imaging, cognitive, CSF and blood-based biomarkers have been proposed for the early detection of AD; their sensitivity and specificity in the symptomatic stages is highly variable and it is difficult to justify their use in even earlier, pre-clinical stages of the disease. Research has identified potentially measurable functional, structural, metabolic and vascular changes in the retina during early stages of AD. Retina offers a distinctively accessible insight into brain pathology and current and developing ophthalmic technologies have provided us with the possibility of detecting and characterising subtle, disease-related changes. Recent human and animal model studies have further provided mechanistic insights into the biochemical pathways that are altered in the retina in disease, including amyloid and tau deposition. This information coupled with advances in molecular imaging has allowed attempts to monitor biochemical changes and protein aggregation pathology in the retina in AD. This review summarises the existing knowledge that informs our understanding of the impact of AD on the retina and highlights some of the gaps that need to be addressed. Future research will integrate molecular imaging innovation with functional and structural changes to enhance our knowledge of the AD pathophysiological mechanisms and establish the utility of monitoring retinal changes as a potential biomarker for AD.
Highlights
Alzheimer’s disease (AD) is a chronic and multifactorial neurodegenerative disorder characterized by progressive cognitive im pairments, behavioral abnormalities and disturbances in circadian rhythm (Ismail et al, 2016)
Since initial reports that highlighted the loss of retinal ganglion cells (RGCs), and particu larly melanopsin expressing RGCs in AD (Sadun and Bassi, 1990; Blanks et al, 1989), several studies have published findings that support the degenerative impact of AD on the inner retinal laminar ar chitecture, including the loss of RGCs in the foveal and para-foveal re gions (Blanks et al, 1996b)
This study suggested that retinal nerve fiber layer (RNFL), IPL and GCL changes might be useful for AD diagnosis, Bruch’s membrane opening–minimum rim width (BMO-MRW) remained unchanged
Summary
Alzheimer’s disease (AD) is a chronic and multifactorial neurodegenerative disorder characterized by progressive cognitive im pairments, behavioral abnormalities and disturbances in circadian rhythm (Ismail et al, 2016). With continuous imaging and CSF biomarker developments, an organized approach was required to bring uniformity in research and diagnostic criteria for AD Towards this end, National Institute of Neurological Disorders and Stroke (NINDS, USA) and Alz heimer’s Association (USA) working group in (2007) recommended neuropsychological assessment as a means to establish cognitive impairment in patients and diagnose them into possible or probable AD cases (Cummings, 2012; Dubois et al, 2007). One potential explanation for these unremarkable outcomes could be the current technological limitations in monitoring subtle brain changes due to inherent difficulties in accessing the intracerebral pathologies Another possibility underlying this failure could be that biochemical alterations are underway in the brain nearly 10–20 years before the development of the clinical syndrome. The ongoing clinical trials, future implications and overlap with other retinal neurodegenerative disorders is discussed
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