[Diabetes mellitus and cognition: is there a link?].

Zina Barrou, Aurélie Lemaire, Jacques Boddaert, Marc Verny
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引用次数: 12

Abstract

The occurrence of diabetes and dementia is very high in older patients. The fact that both conditions are concurrent raises the question of a possible link between the two. Cognitive functions of non-demented patients with diabetes have been extensively studied. In type 1 diabetes, only a mild decrease of the speed of information processing and of the psychomotor efficiency has been shown. Cognitive decline seems to be related to poor metabolic control and not to hypoglycaemia. In older patients with type 2 diabetes, memory and executive functions have been found impaired. Longitudinal studies of the literature have shown that diabetic patients have a higher chance of developing dementia than non-diabetic patient, with a relative risk (RR) between 1.26 and 2.83. The risk of vascular dementia was increased in 3 out of 5 studies, with a RR ranging between 2 and 2.6. With regard to Alzheimer's disease, the results are conflicting. Half of the studies found an increased risk in diabetic patients (RR: 1.3-2). The possible causal mechanisms of dementia in diabetic patients remain hypothetical. MRI studies showed varying degrees of cortical atrophy, cerebral infarcts and deep white matter lesions. In neuropathological studies, senile plaques and neurofibrillary tangle were not found with higher severity in the brain of diabetic patients than in the brain of age-matched controls. Several hypotheses have been raised to explain the relationship between diabetes and cognitive decline. Micro and macrovascular changes in the brain could induce cerebral hypoxia and ischemic conditions resulting in cellular death or white matter lesions. The occurrence of vascular lesions might reduce the threshold at which dementia will occur in Alzheimer disease. The deposition of advanced glycation end products doesn't spare the brain and they have been found in senile plaques, where they can reduce the solubility of proteins such as the beta amyloid and Tau proteins. Some authors favour the hypothesis of a brain insulin resistance because, in a few small studies, insulin was found to improve memory.

[糖尿病和认知:有联系吗?]
老年患者中糖尿病和痴呆的发病率非常高。这两种情况同时发生的事实提出了两者之间可能存在联系的问题。非痴呆型糖尿病患者的认知功能已被广泛研究。在1型糖尿病患者中,仅显示出信息处理速度和精神运动效率的轻微下降。认知能力下降似乎与代谢控制不良有关,而与低血糖无关。在老年2型糖尿病患者中,发现记忆和执行功能受损。文献的纵向研究表明,糖尿病患者发生痴呆的几率高于非糖尿病患者,相对风险(RR)在1.26 ~ 2.83之间。在5项研究中,有3项研究表明血管性痴呆的风险增加,RR在2到2.6之间。关于阿尔茨海默病,结果是相互矛盾的。一半的研究发现糖尿病患者的风险增加(RR: 1.3-2)。糖尿病患者痴呆的可能因果机制仍然是假设的。MRI显示不同程度的皮质萎缩、脑梗死和深部白质病变。在神经病理学研究中,老年斑和神经原纤维缠结在糖尿病患者的大脑中没有发现比在年龄匹配的对照组中更严重。人们提出了几种假说来解释糖尿病和认知能力下降之间的关系。大脑微血管和大血管的改变可引起大脑缺氧和缺血,导致细胞死亡或白质病变。血管病变的发生可能会降低阿尔茨海默病发生痴呆的阈值。晚期糖基化终产物的沉积不会放过大脑,在老年斑中发现了它们,它们可以降低蛋白质的溶解度,如β淀粉样蛋白和Tau蛋白。一些作者支持大脑胰岛素抵抗的假设,因为在一些小的研究中,胰岛素被发现可以改善记忆。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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