Zhang Dong-Mei, Ye Jian-Xin, Mu Jun-Shan, Cui Xiao-Ping
1 Department of Geriatrics, Fuzhou General Hospital of Nanjing Command, PLA and Clinical Medical College of Fujian Medical University, Fuzhou, China.
2 Department of Neurology, Fuzhou General Hospital of Nanjing Command, PLA and Clinical Medical College of Fujian Medical University, Fuzhou, China.
J Geriatr Psychiatry Neurol. 2017 Jan;30(1):50-59. doi: 10.1177/0891988716673466. Epub 2016 Oct 17.
Increase in serum homocysteine is shown to be a potential risk factor for cognitive impairment. Evidence suggests that vitamin B supplementation may reduce cognitive decline by lowering the homocysteine levels. The current meta-analysis evaluated the efficacy of folic acid along with vitamin B12 and/or B6 in lowering homocysteine, thereby attenuating cognitive decline in elderly patients with Alzheimer disease or dementia. Randomized controlled trials (RCTs) comparing the efficacy of folate and B vitamin supplementation in patients with cognitive decline secondary to Alzheimer disease or dementia were identified using the keywords, "homocysteine, hyper-homocysteinemia, B vitamin, vitamin B6, B12, folic acid, cognitive, Alzheimer's disease, and dementia." The outcome measures analyzed were the Mini-Mental State Examination (MMSE) score and serum homocysteine. Of the 77 studies identified, 4 RCTs were included in the current meta-analysis. The baseline characteristics, age, and gender distribution of patients among the 2 groups (supplement vs placebo) were comparable. The results reveal that the intervention group achieved significantly greater reduction in homocysteine levels than the control (pooled difference in means = -3.625, 95% confidence interval [CI] = -5.642 to -1.608, P < .001). However, no significant difference in MMSE (pooled difference in means = 0.027, 95% CI = -0.518 to 0.573, P = 0.921) was observed between the groups. Taken together, vitamin B supplementation was effective in reducing serum homocysteine levels. However, it did not translate into cognitive improvement, indicating that the existing data on vitamin B-induced improvement in cognition by lowering homocysteine levels are conflicting.
血清同型半胱氨酸升高被证明是认知障碍的一个潜在危险因素。有证据表明，补充维生素B可能通过降低同型半胱氨酸水平来减少认知能力下降。当前的荟萃分析评估了叶酸联合维生素B12和/或B6降低同型半胱氨酸水平的疗效，从而减轻老年阿尔茨海默病或痴呆患者的认知能力下降。使用关键词“同型半胱氨酸、高同型半胱氨酸血症、B族维生素、维生素B6、B12、叶酸、认知、阿尔茨海默病和痴呆”确定了比较叶酸和B族维生素补充剂对阿尔茨海默病或痴呆继发认知能力下降患者疗效的随机对照试验（RCT）。分析的结局指标是简易精神状态检查表（MMSE）评分和血清同型半胱氨酸。在确定的77项研究中，4项RCT被纳入当前的荟萃分析。两组（补充剂组与安慰剂组）患者的基线特征、年龄和性别分布具有可比性。结果显示，干预组同型半胱氨酸水平的降低幅度显著大于对照组（合并均值差异=-3.625，95%置信区间[CI]=-5.642至-1.608，P<.001）。然而，两组之间在MMSE方面未观察到显著差异（合并均值差异=0.027，95%CI=-0.518至0.573，P=0.921）。综上所述，补充维生素B可有效降低血清同型半胱氨酸水平。然而，这并未转化为认知功能的改善，表明现有关于维生素B通过降低同型半胱氨酸水平改善认知的数据存在矛盾。
