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Glucose levels during life and neuropathologic findings at autopsy among people never treated for diabetes

机译:从未接受过糖尿病治疗的人一生中的血糖水平和尸检时的神经病理学发现

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摘要

We evaluated associations between glucose and dementia-related neuropathologic findings among people without diabetes treatment history to elucidate mechanisms of glucose’s potential effect on dementia. We used glucose and hemoglobin A1c values to characterize glucose exposures over five years prior to death (primary) and age bands from 55–59 through 80–84 (secondary). Autopsy evaluations included Braak stage for neurofibrillary tangles, CERAD grade for neuritic plaques, macroscopic infarcts including lacunar infarcts, Lewy bodies, cerebral microinfarcts, and hippocampal sclerosis. Of 529 who came to autopsy, we included 430 with no history of diabetes treatment. We found no associations between glucose levels and Braak stage or CERAD grade. There was a suggestion of a relationship between glucose and hippocampal sclerosis, though this was inconsistent across analyses. There was higher risk of Lewy bodies in substantia nigra and locus ceruleus with higher glucose levels in age band analyses. We did not find interactions between glucose levels, neuropathologic findings, and dementia. The mechanism by which glucose may impact dementia risk is still unknown.
机译:我们评估了没有糖尿病治疗史的人中葡萄糖与痴呆相关的神经病理学发现之间的关联,以阐明葡萄糖对痴呆的潜在作用机制。我们使用葡萄糖和血红蛋白A1c值来表征死亡(主要)和55-59岁至80-84(中等)年龄段之前五年内的葡萄糖暴露。尸检评估包括神经纤维缠结的Braak期,神经斑的CERAD分级,包括腔隙性梗死,路易体,脑微梗死和海马硬化的宏观梗死。在进行尸检的529位患者中,我们纳入了430位没有糖尿病治疗史的患者。我们发现血糖水平与Braak分期或CERAD分级之间没有关联。提示葡萄糖与海马硬化之间存在关联,尽管在所有分析中均不一致。在年龄段分析中,黑质和蓝斑中路易体的风险较高,而葡萄糖水平较高。我们没有发现葡萄糖水平,神经病理学发现和痴呆之间存在相互作用。葡萄糖影响痴呆症风险的机制仍然未知。

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