Abstract
Alzheimer’s disease (AD) is the most common form of dementia affecting the growing aging population today, with prevalence expected to rise over the next 35 years. Clinically, patients exhibit a progressive decline in cognition, memory, and social functioning due to deposition of amyloid β (Aβ) protein and intracellular hyperphosphorylated tau protein. These pathological hallmarks of AD are measured either through neuroimaging, cerebrospinal fluid analysis, or diagnosed post-mortem. Importantly, neuropathological progression occurs in the eye as well as the brain, and multiple visual changes have been noted in both human and animal models of AD. The eye offers itself as a transparent medium to cerebral pathology and has thus potentiated the development of ocular biomarkers for AD. The use of non-invasive screening, such as retinal imaging and visual testing, may enable earlier diagnosis in the clinical setting, minimizing invasive and expensive investigations. It also potentially improves disease management and quality of life for AD patients, as an earlier diagnosis allows initiation of medication and treatment. In this review, we explore the evidence surrounding ocular changes in AD and consider the biomarkers currently in development for early diagnosis.
Highlights
The growth in life expectancy and the developing aging population has led to the increased prevalence of chronic diseases, such as Alzheimer’s disease (AD)
We explore the evidence surrounding ocular changes in AD and consider the biomarkers currently in development for early diagnosis
AD is characterized by deposition of extracellular senile plaques, which is composed of amyloid β (Aβ) and intraneuronal neurofibrillary tangles (NFTs), resulting from intracellular aggregates of hyperphosphorylated tau protein detected in the brain [2]
Summary
The growth in life expectancy and the developing aging population has led to the increased prevalence of chronic diseases, such as Alzheimer’s disease (AD). Photoreceptors transmit signals in a neuronal fashion when excited by light and are separated into two main subtypes, rods and cones Bipolar cells transmit this information to retinal ganglion cells (RGCs). Visual symptoms have been well documented in AD, and there is significant evidence to illustrate that ocular pathology occurs as part of the disorder [31, 32] This provides an opportunity to use a minimally invasive approach to examine the pathological features in the brain – through the transparent medium of the eye. Genetic testing in AD has identified three genetic loci, APP, presenilin-1 (PSEN1), and presenilin-2 (PSEN2) as susceptibility genes for early-onset AD (EOAD) and SORL1 and APOE for late-onset AD (LOAD) These genes are useful in predicting the risk of developing AD, their lack of diagnostic specificity and sensitivity and the influence of external environmental factors make them unsuitable as biomarkers for AD [37,38,39]. Changes in visual function have been identified in multiple studies (Table 2) and are being investigated as potential indicators of AD pathology
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