B族维生素,浆果和与年龄有关的神经退行性疾病。

Ethan Balk, Mei Chung, Gowri Raman, Athina Tatsioni, Priscilla Chew, Stanley Ip, Deirdre DeVine, Joseph Lau
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引用次数: 0

摘要

目的:评估B族维生素和浆果及其成分对年龄相关神经认知障碍(主要是阿尔茨海默病(AD)和帕金森病(PD))的影响、关联、作用机制和安全性。数据来源:MEDLINE和CAB摘要。从参考清单和技术专家中确定了其他研究。综述方法:对维生素B1、B2、B6、B12和叶酸以及十几种浆果及其成分进行了评价。评估了人类、动物和体外研究。人类研究的结果是神经认知功能或诊断为AD、认知能力下降、PD或相关疾病。评估了干预研究、饮食摄入与预后之间的关系以及B族维生素水平与预后之间的关系。具体的作用机制在动物和体外研究中进行了评估。从研究设计、人口统计学、干预或预测因素和神经认知结果中提取研究。对研究的质量和适用性进行了分级。结果:在动物实验中,缺乏维生素B1或叶酸通常会导致神经功能障碍;补充B6、B12或叶酸可改善神经认知功能。在动物实验中,叶酸和B12可以预防遗传缺陷,用于模拟AD;硫胺素和叶酸也影响神经血管功能和健康。人体研究通常质量较差。微弱的证据表明补充维生素B1和注射维生素B12可能对阿尔茨海默病有益。维生素B6和叶酸的作用尚不清楚。总的来说,饮食摄入研究不支持维生素B摄入量与AD之间的联系。由于研究设计不佳,评估B族维生素状态的研究大多不充分。总的来说,研究不支持维生素B与年龄相关的神经认知障碍之间的联系。只有一项研究评估了人类食用浆果与帕金森病没有关联。对浆果的动物研究几乎都是由同一个研究小组进行的。一些浆果成分已被证明能影响大脑和神经组织功能。蓝莓和草莓提取物对疾病标志物有保护作用,尽管对神经认知测试的影响不太一致。浆果提取物可以防止与AD相关的化合物的有害影响。不良事件的报道并不常见。当报告时,B族维生素的实际不良事件是罕见和轻微的。结论:目前对B族维生素的研究在很大程度上不足以自信地评估其对与年龄相关的神经认知障碍的作用机制、与疾病的关联或作为补充剂的有效性。补充B族维生素可能对神经认知功能有价值,但证据尚无定论。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
B vitamins and berries and age-related neurodegenerative disorders.

Objectives: To assess the effects, associations, mechanisms of action, and safety of B vitamins and, separately, berries and their constituents on age-related neurocognitive disorders-primarily Alzheimer's (AD) and Parkinson's disease (PD).

Data sources: MEDLINE and CAB Abstracts. Additional studies were identified from reference lists and technical experts.

Review methods: Vitamins B1, B2, B6, B12, and folate, and a dozen types of berries and their constituents were evaluated. Human, animal, and in vitro studies were evaluated. Outcomes of interest from human studies were neurocognitive function or diagnosis with AD, cognitive decline, PD, or related conditions. Intervention studies, associations between dietary intake and outcomes, and associations between B vitamin levels and outcomes were evaluated. Specific mechanisms of action were evaluated in animal and in vitro studies. Studies were extracted for study design, demographics, intervention or predictor, and neurocognitive outcomes. Studies were graded for quality and applicability.

Results: In animal studies, deficiencies in vitamins B1 or folate generally cause neurological dysfunction; supplementation with B6, B12, or folate may improve neurocognitive function. In animal experiments folate and B12 protect against genetic deficiencies used to model AD; thiamine and folate also affect neurovascular function and health. Human studies were generally of poor quality. Weak evidence suggests possible benefits of B1 supplementation and injected B12 in AD. The effects of B6 and folate are unclear. Overall, dietary intake studies do not support an association between B vitamin intake and AD. Studies evaluating B vitamin status were mostly inadequate due to poor study design. Overall, studies do not support an association between B vitamin status and age-related neurocognitive disorders. Only one study evaluated human berry consumption, finding no association with PD. Animal studies of berries have almost all been conducted by the same research group. Several berry constituents have been shown to affect brain and nerve tissue function. Blueberry and strawberry extract were protective of markers of disease, although effects on neurocognitive tests were less consistent. Berry extracts may protect against the deleterious effects of compounds associated with AD. Reporting of adverse events was uncommon. When reported, actual adverse events from B vitamins were rare and minor.

Conclusions: The current research on B vitamins is largely inadequate to confidently assess their mechanisms of action on age-related neurocognitive disorders, their associations with disease, or their effectiveness as supplements. B vitamin supplementation may be of value for neurocognitive function, but the evidence is inconclusive.

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