Abstract
ObjectiveThis study aimed to investigate the risk of Alzheimer’s disease among patients with age-related macular degeneration and its association with confounding comorbidities.MethodThis was a population-based, retrospective cohort study. By accessing data from the National Health Insurance Research Database of Taiwan, we identified 10,578 patients aged 50–100 years who were newly diagnosed with age-related macular degeneration between 2000 and 2012 and 10,578 non- age-related macular degeneration individuals. The comorbidities assessed were osteoporosis, diabetes, cirrhosis, cerebrovascular disease, chronic kidney disease, hypertension, hyperlipidemia, coronary artery disease, and chronic obstructive pulmonary disease.ResultsPatients with age-related macular degeneration had a 1.23-fold increased risk of their condition advancing to Alzheimer’s disease (aHR = 1.23, 95% CI = 1.04–1.46). The younger patients were diagnosed with age-related macular degeneration, the more likely patients got Alzheimer’s disease (50–64 age group: aHR = 1.97, 95% CI = 1.04–3.73; 65–79 age group: aHR = 1.27, 95% CI = 1.02–1.58; 80–100 age group: aHR = 1.06, 95% CI = 0.78–1.45). In addition, there were significantly higher risks of Alzheimer’s disease for patients with cirrhosis (aHR = 1.50, 95% CI = 1.09–2.06) in the age-related macular degeneration cohort than in the non-age-related macular degeneration cohort.ConclusionPatients with age-related macular degeneration may exhibit a higher risk of Alzheimer’s disease than people without age-related macular degeneration.
Highlights
Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by progressive and irreversible cognitive impairment
Patients with age-related macular degeneration had a 1.23-fold increased risk of their condition advancing to Alzheimer’s disease
The younger patients were diagnosed with age-related macular degeneration, the more likely patients got Alzheimer’s disease (50–64 age group: adjusted hazard ratio (aHR) = 1.97, 95% confidence interval (CI) = 1.04–3.73; 65–79 age group: aHR = 1.27, 95% CI = 1.02–1.58; 80–100 age group: aHR = 1.06, 95% CI = 0.78–1.45)
Summary
Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by progressive and irreversible cognitive impairment. The characteristic neuropathological change in AD is the presence of amyloid-beta (Aβ) plaques and neurofibrillary tangles in brain tissues [2, 3]. Over the past two decades, the amyloid cascade hypothesis has been one of the most acceptable theories [4, 5]. Aβ stems from a transmembrane protein of neuronal cells termed amyloid precursor protein (APP). Aβ is generated when APP is sequentially cleaved by β-secretase and γ-secretase [6, 7]. The production and clearance imbalance of Aβ results in abnormal Aβ deposition in the neuropil, which is considered the main cause of synaptic loss and neuronal cell death in AD [8, 9]
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