Department of Epidemiology, Erasmus Medical Center, Rotterdam, the Netherlands.
Department of Ophthalmology, Erasmus Medical Center, Rotterdam, the Netherlands.
JAMA Neurol. 2018 Oct 1;75(10):1256-1263. doi: 10.1001/jamaneurol.2018.1563.
Retinal structures may serve as a biomarker for dementia, but longitudinal studies examining this link are lacking.
To investigate the association of inner retinal layer thickness with prevalent and incident dementia in a general population of Dutch adults.
DESIGN, SETTING, AND PARTICIPANTS: From September 2007 to June 2012, participants from the prospective population-based Rotterdam Study who were 45 years and older and had gradable retinal optical coherence tomography images and at baseline were free from stroke, Parkinson disease, multiple sclerosis, glaucoma, macular degeneration, retinopathy, myopia, hyperopia, and optic disc pathology were included. They were followed up until January 1, 2015, for the onset of dementia.
Inner retinal layer thicknesses (ie, retinal nerve fiber layer [RNFL]) and ganglion cell-inner plexiform layer (GC-IPL) thicknesses measured on optical coherence tomography images.
Odds ratios and hazard ratios for incident dementia per SD decrease in retinal layer thickness adjusted for age, sex, education, and cardiovascular risk factors.
Of 5065 individuals eligible for optical coherence tomography scanning, 3289 (64.9%) (mean [SD] age 68.9 [9.9] years, 1879 [57%] women) were included in the analysis. Of these 3289 individuals, 41 (1.2%) already had dementia. Thinner GC-IPL was associated with prevalent dementia (odds ratio per SD decrease in GC-IPL, 1.37 [95% CI, 0.99-1.90]). No association was found of RNFL with prevalent dementia. During 14 674 person-years of follow-up (mean [SD], 4.5 [1.6] years), 86 individuals (2.6%) developed dementia of whom 68 (2.1%) had Alzheimer disease. Thinner RNFL at baseline was associated with an increased risk of developing dementia (hazard ratio per SD decrease in RNFL, 1.44 [95% CI, 1.19-1.75]), which was similar for Alzheimer disease (hazard ratio, 1.43 [95% CI, 1.15-1.78]). No association was found between GC-IPL thickness and incident dementia (hazard ratio, 1.13 [95% CI, 0.90-1.43]).
Thinner RNFL is associated with an increased risk of dementia, including Alzheimer disease, suggesting that retinal neurodegeneration may serve as a preclinical biomarker for dementia.
视网膜结构可作为痴呆的生物标志物，但缺乏纵向研究来检验这种关联。
在荷兰成年人的一般人群中，调查内视网膜层厚度与现患和新发痴呆的相关性。
设计、地点和参与者：从 2007 年 9 月至 2012 年 6 月，前瞻性基于人群的鹿特丹研究的参与者年龄在 45 岁及以上，可对视网膜光学相干断层扫描图像进行分级，且基线时无中风、帕金森病、多发性硬化症、青光眼、黄斑变性、视网膜病变、近视、远视和视盘病变，随访至 2015 年 1 月 1 日，以记录痴呆的发病情况。
光学相干断层扫描图像上测量的内视网膜层厚度（即视网膜神经纤维层[RNFL]）和神经节细胞内丛状层（GC-IPL）厚度。
按年龄、性别、教育程度和心血管危险因素调整后，每 SD 降低视网膜层厚度与新发痴呆的比值比和风险比。
在符合光学相干断层扫描条件的 5065 名参与者中，有 3289 名（64.9%）（平均[标准差]年龄 68.9[9.9]岁，1879 名[57%]女性）纳入分析。在这 3289 名参与者中，41 名（1.2%）已经患有痴呆症。较薄的 GC-IPL 与现患痴呆症相关（GC-IPL 每 SD 降低的比值比，1.37[95%CI，0.99-1.90]）。RNFL 与现患痴呆症无关。在 14674 人年的随访期间（平均[标准差]，4.5[1.6]年），有 86 人（2.6%）发生痴呆症，其中 68 人（2.1%）患有阿尔茨海默病。基线时较薄的 RNFL 与痴呆症发病风险增加相关（每 SD 降低 RNFL 的风险比，1.44[95%CI，1.19-1.75]），这与阿尔茨海默病相似（风险比，1.43[95%CI，1.15-1.78]）。GC-IPL 厚度与新发痴呆症无关（风险比，1.13[95%CI，0.90-1.43]）。
较薄的 RNFL 与痴呆症风险增加相关，包括阿尔茨海默病，表明视网膜神经退行性变可能是痴呆症的临床前生物标志物。
