Aging Cell：研究发现糖尿病与​​老年痴呆症发病相关

越来越多的证据表明，糖尿病和阿尔茨海默氏病有可能存在某种联系，但糖尿病影响大脑功能和认知的生理机制尚不完全清楚。在一项新的发表在Aging Cell杂志上研究中，索尔克生物研究所研究人员研究表明，糖尿病会加快老化发展，依据阿尔茨海默氏症早在的病理事件。

具体而言，索尔克研究小组发现阿尔茨海默病两个标志，β淀粉样蛋白和tau蛋白存在于糖尿病小鼠大脑中，尤其是在血管周围的细胞中。β淀粉样蛋白的积累被认为是导致阿尔茨海默氏病的主要原因，β淀粉样蛋白与星形胶质细胞相互作用后，星形胶质细胞释放炎症分子破坏神经元。索尔克细胞神经生物学实验室的资深科学家Pamela Maher说：该研究证实了糖尿病、老化和老年痴呆症之间的联系。

1型糖尿病会增加β淀粉样蛋白在大脑中积聚，并导致加速大脑老化。研究结果表明，神经血管系统可能是一个很好的在早期阶段治疗阿尔茨海默氏症的靶点。在美国，阿尔茨海默氏症和糖尿病患者人口以惊人的速度在增加。老年痴呆症影响十分之一的65岁以上老人，近50％的超过85岁以上人受老年痴呆症困扰。同样，超过80％的美国人（约2600万人）是糖尿病患者，其中绝大多数为那些60岁以上的老人。

Maher说她的团队分析了β淀粉样蛋白和tau在小鼠大脑中增加的准确机理，他们的数据表明，星形胶质细胞的变化以及其他促炎性过程和在该过程中做出了贡献。

Antonio Currais说：星形胶质细胞在维持大脑中神经细胞发挥了关键的作用，无论是慢性外周炎症和非酶糖基化反应都与糖尿病相关的，而这些变化可能改变大脑星形胶质细胞的功能，最终导致阿尔茨海默病样病变。

与糖尿病相关的拓展阅读：

• JAMA：研究支持对糖尿病患者进行更强力的抗血小板治疗
• Obes Surg：减重手术可能不能“治愈”糖尿病
• Cell Metab:新的血清标志物提前数年预测糖尿病风险
• Circulation：精氨酸酶抑制剂治疗糖尿病患者并发症
• Diabetologia：维生素D缺乏与1型糖尿病
• JBC：维生素D或可抑制糖尿病患者动脉的阻塞
更多信息请点击：有关糖尿病更多资讯

Diabetes exacerbates amyloid and neurovascular pathology in aging-accelerated mice..

Mounting evidence supports a link between diabetes, cognitive dysfunction, and aging. However, the physiological mechanisms by which diabetes impacts brain function and cognition are not fully understood. To determine how diabetes contributes to cognitive dysfunction and age-associated pathology, we used streptozotocin to induce type 1 diabetes (T1D) in senescence-accelerated prone 8 (SAMP8) and senescence-resistant 1 (SAMR1) mice. Contextual fear conditioning demonstrated that T1D resulted in the development of cognitive deficits in SAMR1 mice similar to those seen in age-matched, nondiabetic SAMP8 mice. No further cognitive deficits were observed when the SAMP8 mice were made diabetic. T1D dramatically increased Aβ and glial fibrillary acidic protein immunoreactivity in the hippocampus of SAMP8 mice and to a lesser extent in age-matched SAMR1 mice. Further analysis revealed aggregated Aβ within astrocyte processes surrounding vessels. Western blot analyses from T1D SAMP8 mice showed elevated amyloid precursor protein processing and protein glycation along with increased inflammation. T1D elevated tau phosphorylation in the SAMR1 mice but did not further increase it in the SAMP8 mice where it was already significantly higher. These data suggest that aberrant glucose metabolism potentiates the aging phenotype in old mice and contributes to early stage central nervous system pathology in younger animals.

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