Kryscio Richard J, Abner Erin L, Cooper Gregory E, Fardo David W, Jicha Gregory A, Nelson Peter T, Smith Charles D, Van Eldik Linda J, Wan Lijie, Schmitt Frederick A
From the Sanders-Brown Center on Aging (R.J.K., E.L.A., G.E.C., G.A.J., P.T.N., C.D.S., L.J.V.E., L.W., F.A.S.), Alzheimer's Disease Center (R.J.K., E.L.A., G.E.C., D.W.F., G.A.J., P.T.N., C.D.S., L.J.V.E., F.A.S.), Departments of Biostatistics (R.J.K., D.W.F.), Statistics (R.J.K., L.W.), Epidemiology (E.L.A.), and Pathology (P.T.N.), Department of Anatomy and Neurobiology, College of Medicine (L.J.V.E.), and Department of Neurology, College of Medicine (G.A.J., C.D.S., F.A.S.), University of Kentucky, Lexington; and Baptist Neurology Center (G.E.C.), Lexington, KY.
Neurology. 2014 Oct 7;83(15):1359-65. doi: 10.1212/WNL.0000000000000856. Epub 2014 Sep 24.
We assessed salience of subjective memory complaints (SMCs) by older individuals as a predictor of subsequent cognitive impairment while accounting for risk factors and eventual neuropathologies.
Subjects (n = 531) enrolled while cognitively intact at the University of Kentucky were asked annually if they perceived changes in memory since their last visit. A multistate model estimated when transition to impairment occurred while adjusting for intervening death. Risk factors affecting the timing and probability of an impairment were identified. The association between SMCs and Alzheimer-type neuropathology was assessed from autopsies (n = 243).
SMCs were reported by more than half (55.7%) of the cohort, and were associated with increased risk of impairment (unadjusted odds ratio = 2.8, p < 0.0001). Mild cognitive impairment (dementia) occurred 9.2 (12.1) years after SMC. Multistate modeling showed that SMC reporters with an APOE ε4 allele had double the odds of impairment (adjusted odds ratio = 2.2, p = 0.036). SMC smokers took less time to transition to mild cognitive impairment, while SMC hormone-replaced women took longer to transition directly to dementia. Among participants (n = 176) who died without a diagnosed clinical impairment, SMCs were associated with elevated neuritic amyloid plaques in the neocortex and medial temporal lobe.
SMC reporters are at a higher risk of future cognitive impairment and have higher levels of Alzheimer-type brain pathology even when impairment does not occur. As potential harbingers of future cognitive decline, physicians should query and monitor SMCs from their older patients.
我们评估了老年人主观记忆主诉（SMC）的显著性，将其作为后续认知障碍的预测指标，同时考虑了风险因素和最终的神经病理学情况。
肯塔基大学招募的认知功能完好的受试者（n = 531）每年被询问自上次就诊以来是否察觉到记忆变化。一个多状态模型估计了向认知障碍转变的时间，同时对中间死亡情况进行了调整。确定了影响认知障碍发生时间和概率的风险因素。从尸检（n = 243）中评估了SMC与阿尔茨海默病型神经病理学之间的关联。
超过一半（55.7%）的队列报告有SMC，且与认知障碍风险增加相关（未调整的优势比 = 2.8，p < 0.0001）。轻度认知障碍（痴呆）在出现SMC后9.2（12.1）年发生。多状态建模显示，携带APOE ε4等位基因的SMC报告者发生认知障碍的几率翻倍（调整后的优势比 = 2.2，p = 0.036）。有SMC的吸烟者向轻度认知障碍转变所需时间更短，而接受激素替代治疗的有SMC的女性直接转变为痴呆所需时间更长。在未被诊断为临床认知障碍而死亡的参与者（n = 176）中，SMC与新皮质和内侧颞叶神经炎性淀粉样斑块增多相关。
报告有SMC的人未来发生认知障碍的风险更高，即使未发生认知障碍，其阿尔茨海默病型脑病理学水平也更高。作为未来认知衰退的潜在预兆，医生应询问并监测老年患者的SMC。
