前期糖尿病，而非 2 型糖尿病，与中老年时期的脑淀粉样蛋白有关。
Pre-Diabetes, but not Type 2 Diabetes, Is Related to Brain Amyloid in Late Middle-Age.
机构信息
Department of Medicine, College of Physicians and Surgeons, Columbia University Irving Medical Center (CUIMC), New York, NY, USA.
Department of Epidemiology, Joseph P. Mailman School of Public Health, CUIMC, New York, NY, USA.
出版信息
J Alzheimers Dis. 2020;75(4):1241-1252. doi: 10.3233/JAD-200232.
BACKGROUND
Type 2 diabetes is a dementia risk factor, but its relation to Alzheimer's disease (AD), the most common cause of dementia, is unclear.
OBJECTIVE
Our primary objective was to examine the association of pre-diabetes and type 2 diabetes with brain amyloid-β (Aβ), the putative main culprit of AD. Our secondary objective was to examine the association of pre-diabetes and type 2 diabetes with neurodegeneration, cerebrovascular disease (CVD), and memory performance.
METHODS
We conducted a cross-sectional study of 350 late middle-aged Hispanics without dementia in New York City. We classified diabetes status as normal glucose tolerance (NGT), pre-diabetes, and type 2 diabetes following American Diabetes Association criteria. Brain Aβ was ascertained as global Aβ standardized value uptake ratio using PET with 18F-Florbetaben. Neurodegeneration was operationalized as cortical thickness in regions affected by AD using MRI. CVD was operationalized as white matter hyperintensity volume (WMH) on MRI, and memory as performance with the selective reminding test (SRT).
RESULTS
Mean age was 64.15±3.34 years, 72.00% were women, and 35.43% were APOEɛ4 carriers. Pre-diabetes, but not type 2 diabetes, was associated with higher Aβ compared with NGT. Type 2 diabetes treatment was related to lower Aβ. Type 2 diabetes was related to lower cortical thickness, higher WMH, and lower SRT score.
CONCLUSION
Pre-diabetes, but not type 2 diabetes, is associated with higher brain Aβ in late middle age, and this observation could be explained by the relation of diabetes treatment with lower brain Aβ. Whether type 2 diabetes treatment lowers brain Aβ requires further study.
背景
2 型糖尿病是痴呆的一个危险因素，但它与阿尔茨海默病（AD）的关系尚不清楚，AD 是痴呆的最常见病因。
目的
我们的主要目的是研究糖尿病前期和 2 型糖尿病与脑β淀粉样蛋白（Aβ）的关系，Aβ 是 AD 的主要罪魁祸首。我们的次要目的是研究糖尿病前期和 2 型糖尿病与神经退行性变、脑血管疾病（CVD）和记忆表现的关系。
方法
我们在纽约市进行了一项横断面研究，纳入了 350 名无痴呆的中老年西班牙裔人群。我们根据美国糖尿病协会的标准，将糖尿病状态分为正常糖耐量（NGT）、糖尿病前期和 2 型糖尿病。使用 18F-氟比他滨 PET 检测脑 Aβ，确定为全球 Aβ标准化摄取比值。使用 MRI 检测 AD 受累区域的皮质厚度来衡量神经退行性变。使用 MRI 上的白质高信号体积（WMH）来衡量 CVD，使用选择性提醒测试（SRT）来衡量记忆。
结果
平均年龄为 64.15±3.34 岁，72.00%为女性，35.43%为 APOEɛ4 携带者。与 NGT 相比，糖尿病前期而非 2 型糖尿病与更高的 Aβ 相关。2 型糖尿病的治疗与较低的 Aβ相关。2 型糖尿病与较低的皮质厚度、较高的 WMH 和较低的 SRT 评分相关。
结论
糖尿病前期而非 2 型糖尿病与中老年人群的脑 Aβ 升高相关，这种观察结果可能与糖尿病治疗与较低的脑 Aβ 相关。2 型糖尿病治疗是否降低脑 Aβ 需要进一步研究。
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