It has been more than 100 years since Alois Alzheimer identified Alzheimer disease (AD), and almost 40 years since the role of amyloid-β (Aβ) and tau proteins, 2 key molecular factors in the AD pathophysiologic patterns, were identified.1 Alzheimer disease is now recognized as a multifaceted process that progresses along a continuum with a commonly defined starting point being the accumulation of the Aβ biomarker demonstrated on positron emission tomography (PET) or cerebrospinal fluid analysis. The epidemic of AD has already decreased the life expectancy in the US,2 adding to the urgency to identify a noninvasive biomarker to easily detect not only those with symptomatic AD, but also those with preclinical AD for whom lifestyle modifications, such as diet, exercise, and cognitive engagement, may delay onset. The retina holds promise in being able to provide such a biomarker, yet challenges remain, ranging from our evolving understanding of underlying AD pathophysiologic characteristics to current limitations of retinal imaging.
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Grewal DS, Fekrat S. Structural and Functional Retinal Changes in Preclinical Alzheimer Disease. JAMA Ophthalmol. 2021;139(5):556–557. doi:10.1001/jamaophthalmol.2021.0319
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