دانلود رایگان مقاله انگلیسی علائم شبکیه و کاهش 20 ساله علائم شناختی در خطر تصلب شرایین در جامعه مطالعات - NCBI 2018

Abstract

Objective To test the hypothesis that retinal vascular signs are associated with greater cognitive decline over 20 years in 12,317 men and women 50 to 73 years of age at baseline. Methods A composite cognitive score was created with 3 neuropsychological tests measured at 3 time points (1990–1992 to 2011–2013). Retinal signs were measured with fundus photography (1993–1995). Differences in cognitive change by retinal signs status were estimated with linear mixed models. Cognitive scores were imputed for living participants with incomplete cognitive testing. Results In multivariable-adjusted analyses that controlled for attrition, loss of vascular integrity (retinopathy and its components) was associated with greater 20-year decline (difference in 20-year cognitive change for moderate/severe vs no retinopathy −0.53 SD, 95% confidence interval −0.74 to −0.33). Estimated differences were similar in participants with and without diabetes mellitus and in white and black participants. Conclusions Retinopathy was associated with accelerated rates of 20-year cognitive decline. These findings support the exploration of more sensitive measures in the eye such as optical coherence tomography angiography, which may provide surrogate indexes of microvascular lesions relevant to cognitive decline in older adults. GLOSSARY ARIC = Atherosclerosis Risk in Communities; CHD = coronary heart disease; CI = confidence interval; CRAE = central retinal arteriolar equivalent; ETDRS = Early Treatment Diabetic Retinopathy Study; OR = odds ratio; 3MS = Modified Mini-Mental State Examination.

Discussion

In this study of 12,317 men and women (age 50–73 years, 22% black), measures of loss of vascular integrity (retinopathy) were associated with faster 20-year cognitive decline. In analyses adjusted for attrition, estimates of the difference in rates of 20-year cognitive change for moderate/severe retinopathy and its components ranged from −0.21 to −0.57 SD. Measures of arteriolar changes (CRAE and focal narrowing) were associated with declines in demographicadjusted models but not after full adjustment, perhaps because these signs are simply reflective of the risk factors included in the model. Associations in our study were similar in blacks and whites and in persons with and without diabetes mellitus. To put the magnitude of these associations in perspective, a previous study estimated the 20-year effect of baseline diabetes mellitus on cognitive decline using the same methods to account for informative censoring to be −0.21 SD (95% CI −0.31 to −0.12).19 If retinal signs are adequate surrogates for homologous changes in the brain, these differences could represent reasonable estimates of the otherwise not estimable net contribution of cerebral small vessel disease (including microinfarction) to cognitive decline in older adults, independently of declines due to Alzheimer disease and other processes with a pathogenesis that is not primarily vascular.