The University of Sydney, Faculty of Science, School of Psychology, Sydney, New South Wales, Australia; The University of Sydney, Brain and Mind Centre, Sydney, New South Wales, Australia; Woolcock Institute of Medical Research, Centre for Sleep and Chronobiology, The University of Sydney, Sydney, New South Wales, Australia.
The University of Sydney, Charles Perkins Centre, Sydney, New South Wales, Australia; The University of Sydney, Faculty of Medicine and Health, The Boden Collaboration for Obesity, Nutrition, Exercise and Eating Disorders, Sydney, New South Wales, Australia.
Diabetes Res Clin Pract. 2022 Feb;184:109178. doi: 10.1016/j.diabres.2021.109178. Epub 2021 Dec 24.
Diabetes is an established risk factor for dementia. This study aimed to examine the relationship between various cognitive domains, brain oxidative stress and markers of diabetes in older adults at risk for dementia.
Older adults at risk for dementia underwent comprehensive neuropsychological and medical assessment. At risk was defined as those with subjective and/or objective cognitive impairment. Pre-diabetes and type 2 diabetes were defined using American Diabetes Association definitions for fasting blood glucose and HbA1c. Brain oxidative stress as indicated by glutathione (GSH) was assessed via magnetic resonance spectroscopy in the anterior cingulate cortex.
One-hundred and forty-seven older adults completed a neuropsychological assessment and fasting blood sample with 63 also undergoing magnetic resonance spectroscopy. Those with pre-diabetes/diabetes according to FBG had impaired memory retention, set-shifting and response inhibition, compared to those with normal blood glucose. In contrast, there were no significant differences in any cognitive outcome using the HbA1c definition. Increasing glucose and HbA1c levels were associated with reduced GSH concentration in the anterior cingulate.
This study demonstrates that in older adults at risk for dementia, having pre-diabetes or diabetes is associated with impaired memory and executive dysfunction. It also highlights the potential role of oxidative stress as a pathophysiological mechanism that may underpin the link between diabetes and cognitive dysfunction.
糖尿病是痴呆的既定危险因素。本研究旨在探讨老年痴呆高危人群各认知领域、大脑氧化应激与糖尿病标志物之间的关系。
老年痴呆高危人群接受了全面的神经心理学和医学评估。高危定义为有主观和/或客观认知障碍的人群。使用美国糖尿病协会(ADA)的空腹血糖和糖化血红蛋白(HbA1c)定义来界定糖尿病前期和 2 型糖尿病。通过磁共振波谱在扣带回前部评估大脑氧化应激的标志物谷胱甘肽(GSH)。
147 名老年人完成了神经心理学评估和空腹血样采集,其中 63 人还进行了磁共振波谱检查。与血糖正常者相比,根据 FBG 诊断为糖尿病前期/糖尿病的患者记忆力、转换能力和反应抑制能力受损。相比之下,使用 HbA1c 定义时,任何认知结果均无显著差异。葡萄糖和 HbA1c 水平的升高与扣带回前部 GSH 浓度的降低有关。
本研究表明,在老年痴呆高危人群中,糖尿病前期或糖尿病与记忆和执行功能障碍有关。它还强调了氧化应激作为潜在的病理生理机制的作用,这可能是糖尿病与认知功能障碍之间联系的基础。