Namioka Nayuta, Hanyu Haruo, Hirose Daisuke, Hatanaka Hirokuni, Sato Tomohiko, Shimizu Soichiro
Department of Geriatric Medicine, Tokyo Medical University, Tokyo, Japan.
Geriatr Gerontol Int. 2017 Jun;17(6):913-918. doi: 10.1111/ggi.12804. Epub 2016 Jun 14.
Dementia is closely connected with frailty, and these two conditions are common in older adults. However, the biological mechanism that causes frailty in patients with Alzheimer's disease (AD) is not fully understood. We determined whether oxidative stress and inflammatory mechanisms could be associated with physical frailty in patients with AD.
We studied 140 elderly outpatients with mild-to-moderate AD. Frailty status was determined according to the presence of the following five measurable characteristics: weight loss, exhaustion, low physical activity, slowness and weakness. We measured oxidative stress markers, including plasma levels of diacron reactive oxygen metabolite and biological anti-oxidant potential, endogenous plasma anti-oxidants, such as albumin, bilirubin and uric acid, and urinary 8-hydroxy-2'-deoxyguanosine (8-OHdG) and 8-epiPGF2α (8-isoprostane), and inflammatory markers, including interleukin-6 and tumor necrosis factor-α.
Among patients, 44 (31%) were non-frail, 62 (44%) were prefrail and 34 (24%) were frail. Frail and prefrail patients were older, more likely to be women and had more comorbid medical conditions than non-frail patients. Frail or prefrail patients showed significantly higher diacron reactive oxygen metabolite and lower biological anti-oxidant potential levels, a significant decrease in bilirubin, a significant increase in urinary 8-OHdG and 8-isoprostane levels, and a significantly higher interleukin-6 level, in contrast to non-frail patients.
Physical frailty is common in old and female AD patients with comorbid medical diseases. The present results strongly suggest that oxidative stress and inflammation are involved in the pathophysiology of frailty status in individuals with AD. Geriatr Gerontol Int 2017; 17: 913-918.
痴呆与身体虚弱密切相关，这两种情况在老年人中很常见。然而，导致阿尔茨海默病（AD）患者身体虚弱的生物学机制尚未完全明确。我们确定氧化应激和炎症机制是否与AD患者的身体虚弱有关。
我们研究了140例轻度至中度AD老年门诊患者。根据以下五个可测量特征的存在情况确定虚弱状态：体重减轻、疲惫、体力活动少、行动迟缓及虚弱。我们测量了氧化应激标志物，包括血浆中戴克隆活性氧代谢产物水平和生物抗氧化潜能、内源性血浆抗氧化剂如白蛋白、胆红素和尿酸，以及尿8-羟基-2'-脱氧鸟苷（8-OHdG）和8-表前列腺素F2α（8-异前列腺素），以及炎症标志物，包括白细胞介素-6和肿瘤坏死因子-α。
在患者中，44例（31%）非虚弱，62例（44%）为虚弱前期，34例（24%）虚弱。与非虚弱患者相比，虚弱和虚弱前期患者年龄更大，更可能为女性，且合并症更多。与非虚弱患者相比，虚弱或虚弱前期患者的戴克隆活性氧代谢产物水平显著更高，生物抗氧化潜能水平更低，胆红素显著降低，尿8-OHdG和8-异前列腺素水平显著升高，白细胞介素-6水平显著更高。
身体虚弱在患有合并症的老年女性AD患者中很常见。目前的结果强烈表明，氧化应激和炎症参与了AD患者虚弱状态的病理生理过程。《老年医学与老年病学国际杂志》2017年；17：913 - 918。
