Docosahexaenoic acid supplementation and cognitive decline in Alzheimer disease: a randomized trial.
Docosahexaenoic acid supplementation and cognitive decline in Alzheimer disease: a randomized trial.
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DOI：
10.1001/jama.2010.1510
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发表时间：
2010-11-03
期刊：
影响因子：
--
通讯作者：
Aisen PS
中科院分区：
文献类型：
--
作者：
Quinn JF;Raman R;Thomas RG;Yurko-Mauro K;Nelson EB;Van Dyck C;Galvin JE;Emond J;Jack CR Jr;Weiner M;Shinto L;Aisen PS
二十二碳六烯酸（DHA）是大脑中最丰富的长链多不饱和脂肪酸。流行病学研究表明，DHA的消费与阿尔茨海默病的发病率降低有关。动物研究表明，口服DHA可减少阿尔茨海默病样脑病变。确定补充DHA是否减缓阿尔茨海默病患者的认知和功能下降。2007年11月至2009年5月，在美国阿尔茨海默病合作研究的51个临床研究中心进行了一项关于轻度至中度阿尔茨海默病（简易精神状态检查评分，14-26）患者补充DHA的随机、双盲、安慰剂对照试验。参与者被随机分配到剂量为2 g/d的藻类DHA或相同的安慰剂组（60%分配到DHA组，40%分配到安慰剂组）。治疗持续时间为18个月。阿尔茨海默病评估量表（ADAS-cog）认知子量表的变化和临床痴呆评定（CDR）方框总和的变化。脑萎缩率也通过体积磁共振成像在参与者的子样本（n = 102）中确定。共有402名受试者被随机分组，共有295名受试者在服用研究药物（DHA：171;安慰剂：124）的同时完成了试验。补充DHA对ADAS-cog评分的变化率没有有益的影响，在18个月期间，DHA组的ADAS-cog评分平均增加了7.98分（95%置信区间[CI]，6.51-9.45分），而安慰剂组为8.27分（95% CI，6.72-9.82分）（线性混合效应模型：P = 0.41）。在18个月期间，DHA组的CDR总分增加了2.87分（95%CI，2.44-3.30分），而安慰剂组为2.93分（95%CI，2.44-3.42分）（线性混合效应模型：P = 0.68）。在参与者的亚群中（DHA：53;安慰剂：49），脑萎缩率不受DHA治疗的影响。DHA组的个体总脑体积平均下降24.7 cm 3（95% CI，21.4-28.0 cm3），1.32%（95% CI，1.14%-1.50%）与24.0 cm 3相比每年体积下降（95% CI，20-28 cm 3），每年体积下降1.29%（95% CI，1.07%-1.51%）（P = 0.79）。与安慰剂相比，补充DHA并没有减缓轻度至中度阿尔茨海默病患者的认知和功能下降速度。
Docosahexaenoic acid (DHA) is the most abundant long-chain polyunsaturated fatty acid in the brain. Epidemiological studies suggest that consumption of DHA is associated with a reduced incidence of Alzheimer disease. Animal studies demonstrate that oral intake of DHA reduces Alzheimer-like brain pathology. To determine if supplementation with DHA slows cognitive and functional decline in individuals with Alzheimer disease. A randomized, double-blind, placebo-controlled trial of DHA supplementation in individuals with mild to moderate Alzheimer disease (Mini-Mental State Examination scores, 14–26) was conducted between November 2007 and May 2009 at 51 US clinical research sites of the Alzheimer’s Disease Cooperative Study. Participants were randomly assigned to algal DHA at a dose of 2 g/d or to identical placebo (60% were assigned to DHA and 40% were assigned to placebo). Duration of treatment was 18 months. Change in the cognitive subscale of the Alzheimer’s Disease Assessment Scale (ADAS-cog) and change in the Clinical Dementia Rating (CDR) sum of boxes. Rate of brain atrophy was also determined by volumetric magnetic resonance imaging in a subsample of participants (n = 102). A total of 402 individuals were randomized and a total of 295 participants completed the trial while taking study medication (DHA: 171; placebo: 124). Supplementation with DHA had no beneficial effect on rate of change on ADAS-cog score, which increased by a mean of 7.98 points (95% confidence interval [CI], 6.51–9.45 points) for the DHA group during 18 months vs 8.27 points (95% CI, 6.72–9.82 points) for the placebo group (linear mixed-effects model: P = .41). The CDR sum of boxes score increased by 2.87 points (95% CI, 2.44–3.30 points) for the DHA group during 18 months compared with 2.93 points (95% CI, 2.44–3.42 points) for the placebo group (linear mixed-effects model: P = .68). In the subpopulation of participants (DHA: 53; placebo: 49), the rate of brain atrophy was not affected by treatment with DHA. Individuals in the DHA group had a mean decline in total brain volume of 24.7 cm3 (95% CI, 21.4–28.0 cm3) during 18 months and a 1.32% (95% CI, 1.14%–1.50%) volume decline per year compared with 24.0 cm3 (95% CI, 20–28 cm3) for the placebo group during 18 months and a 1.29% (95% CI, 1.07%–1.51%) volume decline per year (P = .79). Supplementation with DHA compared with placebo did not slow the rate of cognitive and functional decline in patients with mild to moderate Alzheimer disease.
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