根據(jù)The Archives of Neurology網(wǎng)上公布的一項(xiàng)研究，一種由稱為脂聯(lián)素的內(nèi)臟脂肪衍生而來的激素在女性各種原因癡呆和阿爾茨海默?。ˋD）的發(fā)生中可能起一個(gè)危險(xiǎn)因素的作用,。
據(jù)估計(jì)，在今后20年,，全球受癡呆癥影響的人數(shù)會(huì)比當(dāng)前的約3600萬人翻番，這是文章中作者提供的背景信息。AD是最常見的癡呆癥形式,。作者寫的數(shù)據(jù)表明了胰島素抵抗與炎癥間的聯(lián)系及癡呆癥發(fā)展,，其中胰島素抵抗與炎癥間的聯(lián)系以II型糖尿病為標(biāo)志,。"脂聯(lián)素是可能有助于AD發(fā)病和各種原因癡呆癥的另外一個(gè)潛在因素,。脂聯(lián)素是一種來源于內(nèi)臟脂肪的激素,，這種內(nèi)臟脂肪使機(jī)體對胰島素敏感，脂聯(lián)素具有抗炎特性,，并在糖與脂代謝中發(fā)揮作用。"
來自波士頓塔夫斯大學(xué)TUFTS大學(xué)人類老年?duì)I養(yǎng)研究中心脂質(zhì)代謝實(shí)驗(yàn)室的Thomas M. van Himbergen博士和同事們測定了患者血漿中血糖,、胰島素,，糖化白蛋白、C反應(yīng)蛋白,、脂蛋白相關(guān)磷脂酶A 2以及脂聯(lián)素水平,，他們是弗雷明漢心臟研究第19次兩年一次檢查（1985-1988）的患者。
其中840例（541名婦女,，平均年齡76年）患者平均13年隨訪一次,，評價(jià)AD和癡呆癥發(fā)展的各種指征,。在這期間,，159例發(fā)生癡呆，其中包括125例AD,。在調(diào)整其他癡呆癥的危險(xiǎn)因素后（年齡,，載脂蛋白E基因型，低血漿二十二碳六烯酸,，體重變化）,，只有女性脂聯(lián)素是與各種原因的癡呆和AD風(fēng)險(xiǎn)性增加相關(guān),。
"已經(jīng)很確定的是，在AD患者大腦中胰島素信號功能失調(diào),，因?yàn)橹?lián)素增強(qiáng)胰島素敏感性,，人們還期待防止認(rèn)知能力下降的有益作用"，作者寫道,。"但是，我們的數(shù)據(jù)暗示,，升高的脂聯(lián)素水平與女性癡呆癥和AD增加的風(fēng)險(xiǎn)性相關(guān)。"
作者總結(jié)如下："脂聯(lián)素的一個(gè)主要特點(diǎn)是,，它已被證明在胰島素敏感性中發(fā)揮作用,，因此可能成為II型糖尿病(T2D)治療的一個(gè)靶點(diǎn),。令人驚訝的是,，高脂聯(lián)素水平被發(fā)現(xiàn)是各種原因和血管死亡率的一個(gè)預(yù)測因素,。在死亡率調(diào)查發(fā)現(xiàn)的同時(shí),，目前的研究表明，升高的脂聯(lián)素水平也是女性各種原因癡呆和AD的一個(gè)獨(dú)立預(yù)測因素,。"（生物谷bioon.com）
doi:10.1001/archneurol.2011.670
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Biomarkers for Insulin Resistance and Inflammation and the Risk for All-Cause Dementia and Alzheimer Disease
Thomas M. van Himbergen, PhD; Alexa S. Beiser, PhD; Masumi Ai, MD; Sudha Seshadri, MD; Seiko Otokozawa, MT; Rhoda Au, PhD; Nuntakorn Thongtang, MD;Philip A. Wolf, MD; Ernst J. Schaefer, MD
ABSTRACT Objective To investigate the contribution of biomarkers of glucose homeostasis (adiponectin, glucose, glycated albumin, and insulin levels) and inflammation (high-sensitivity C-reactive protein and lipoprotein-associated phospholipase A2 levels) to the risk of developing Alzheimer disease (AD) and all-cause dementia. Design Prospective cohort study. Setting Dementia-free Framingham Heart Study participants had sera measured for these biomarkers at the 19th biennial examination (1985-1988) and were followed up prospectively for the development of AD and all-cause dementia. Participants Eight hundred forty (541 women, median age of 76 years) subjects participated in the study. Main Outcome Measures We used sex-pooled and sex-specific multivariable Cox proportional hazards models adjusted for age, education, body mass index, recent change in weight, APOE 4 allele status, and plasma docosahexaenoic acid levels to determine association of these biomarkers with the development of all-cause dementia and AD. Results Over a mean follow-up period of 13 years, 159 persons developed dementia (including 125 with AD). After adjustment for other risk factors, only adiponectin in women was associated with an increased risk of all-cause dementia (hazard ratio [HR], 1.29; 95% confidence interval [CI], 1.00-1.66; P = .054) and AD (HR, 1.33; 95% CI, 1.00-1.76; P = .050) per 1-SD increase in adiponectin level. Women with baseline adiponectin values more than the median had a higher risk of all-cause dementia (HR, 1.63; 95% CI, 1.03-2.56; P = .04) and AD (HR, 1.87; 95% CI, 1.13-3.10; P = .01) as compared with those with values less than the median. Conclusion In women, increased plasma adiponectin levels are an independent risk factor for the development of both all-cause dementia and AD
