The link between non-demented type 2 diabetes mellitus (T2DM) and different types of cognitive impairment is controversial. By controlling for co-morbidities such as cerebral macrovascular and microvascular changes, cerebral atrophy, amyloid burden, hypertension or hyperlipidemia, the current study investigated the cerebral blood flow of T2DM individuals as compared to cognitively impaired subjects recruited from a memory clinic.

15 healthy control (71.8 ± 6.1 years), 18 T2DM (62.5 ± 3.7 years), as well as 8 Subjective Cognitive Decline (69.5 ± 7.5 years), 12 Vascular Dementia (79.3 ± 4.2 years) and 17 Alzheimer’s Disease (75.1 ± 8.2 years) underwent multi-parametric MRI brain scanning. Subjects with T2DM and from the memory clinic also had 18-F Flutametamol PET-CT scanning to look for any amyloid burden. Pseudocontinuous Arterial Spin Labeling (PCASL), MR Angiography Head, 3D FLAIR and 3D T1-weighted sequences were used to quantify cerebral blood flow, cerebrovascular changes, white matter hyperintensities and brain atrophy respectively. Vascular risk factors were retrieved from the medical records. The 37 subjects from memory clinic were classified into subjective cognitive decline (SCD), vascular dementia (VD) and Alzheimer’s disease (AD) subgroups by a multi-disciplinary panel consisting of a neuroradiologist, and 2 geriatricians.

Absolute cortical CBF in our cohort of T2DM, SCD, VD and AD was significantly decreased (p < 0.01) as compared to healthy controls (HC) in both whole brain and eight paired brain regions, after age, normalized grey matter volume and gender adjustment and Bonferroni correction.

Subgroup analysis between T2DM, SCD, VD, and AD revealed that CBF of T2DM was not significantly different from AD, VD or SCD. By controlling for co-morbidities, impaired cortical CBF in T2DM was not related to microangiopathy or amyloid deposition, but to the interaction of triple risk factors (such as diabetes mellitus, hypertension, and hyperlipidemia).

There was statistically significant negative correlation (p ≤ 0.05) between adjusted CBF and HbA1c in all brain regions of T2DM and HC (with partial correlation ranging from −0.30 to −0.46).

Taken together, altered cerebral blood flow in T2DM might be related to disruption of cerebrovascular autoregulation related to vascular risk factors, and such oligemia occurred before clinical manifestation due to altered glycemic control.

非痴呆型2型糖尿病（T2DM）与不同类型的认知障碍之间的联系存在争议。通过控制诸如脑大血管和微血管变化，脑萎缩，淀粉样蛋白负荷，高血压或高血脂症等合并症，与从记忆诊所招募的患有认知障碍的受试者相比，本研究调查了T2DM个体的脑血流量。

15位健康对照者（71.8±6.1年），18位T2DM（62.5±3.7年），8位主观认知下降（69.5±7.5年），12位血管性痴呆（79.3±4.2年）和17位阿尔茨海默氏病（75.1±8.2岁）年）进行了多参数MRI脑部扫描。患有T2DM且来自记忆诊所的受试者也进行了18-F Flutametamol PET-CT扫描，以寻找任何淀粉样蛋白负担。伪连续动脉自旋标记（PCASL），MR血管造影头，3D FLAIR和3D T1加权序列分别用于定量脑血流量，脑血管变化，白质高信号和脑萎缩。从病历中检索出血管危险因素。记忆诊所的37名受试者被分为主观认知能力下降（SCD），

 在年龄，正常灰质体积和性别调整后，我们的T2DM，SCD，VD和AD队列的绝对皮层CBF与健康对照组（HC）相比，在全脑和八个配对脑区均显着降低（p <0.01）和Bonferroni校正。

T2DM，SCD，VD和AD之间的亚组分析显示，T2DM的CBF与AD，VD或SCD并无显着差异。通过控制合并症，T2DM的皮质CBF受损与微血管病或淀粉样蛋白沉积无关，但与三重危险因素（如糖尿病，高血压和高脂血症）的相互作用有关。

在T2DM和HC的所有脑区域中，调整后的CBF与HbA1c之间存在统计学上的显着负相关（p≤0.05）（部分相关范围为-0.30至-0.46）。

两者合计，T2DM中脑血流量的改变可能与与血管危险因素有关的脑血管自动调节的破坏有关，并且这种低血糖症是由于血糖控制改变而在临床表现之前发生的。