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Potential of coconut oil and medium chain triglycerides in the prevention and treatment of Alzheimer's disease.
Mechanisms of Ageing and Development ( IF 5.3 ) Pub Date : 2020-01-15 , DOI: 10.1016/j.mad.2020.111209
Pratishtha Chatterjee 1 , Malika Fernando 2 , Binosha Fernando 3 , Cintia B Dias 4 , Tejal Shah 5 , Renuka Silva 2 , Shehan Williams 6 , Steve Pedrini 3 , Heidi Hillebrandt 7 , Kathryn Goozee 8 , Edward Barin 9 , Hamid R Sohrabi 5 , Manohar Garg 10 , Stephen Cunnane 11 , Ralph N Martins 12
Affiliation  

Alzheimer's disease (AD) is the most common form of dementia. Currently, there is no effective medication for the prevention or treatment of AD. This has led to the search for alternative therapeutic strategies. Coconut oil(CO) has a unique fatty acid composition that is rich in medium chain fatty acids(MCFA), a major portion of which directly reaches the liver via the portal vein, thereby bypassing the lymphatic system. Given that brain glucose hypometabolism is a major early hallmark of AD, detectable well before the onset of symptoms, ketone bodies from MCFA metabolism can potentially serve as an alternative energy source to compensate for lack of glucose utilisation in the brain. Additionally, neuroprotective antioxidant properties of CO have been attributed to its polyphenolic content. This review discusses how the metabolism of CO and MCFA may aid in compensating the glucose hypometabolism observed in the AD brain. Furthermore, we present the current evidence of the neuroprotective properties of CO on cognition, amyloid-β pathogenicity, inflammation and oxidative stress. The current review addresses the influence of CO/MCFA on other chronic disorders that are risk factors for AD, and addresses existing gaps in the literature regarding the use of CO/MCFA as a potential treatment for AD.

中文翻译:

椰子油和中链甘油三酸酯在预防和治疗阿尔茨海默氏病中的潜力。

阿尔茨海默氏病(AD)是痴呆症的最常见形式。当前,没有有效的药物用于预防或治疗AD。这导致寻找替代治疗策略。椰子油(CO)具有独特的脂肪酸成分,富含中链脂肪酸(MCFA),其中大部分通过门静脉直接到达肝脏,从而绕过淋巴系统。鉴于脑葡萄糖代谢低下是AD的主要早期特征,可以在症状发作之前就检测到,因此MCFA代谢产生的酮体可以作为替代能源来弥补大脑中葡萄糖的缺乏。此外,CO的神经保护抗氧化特性归因于其多酚含量。这篇评论讨论了CO和MCFA的代谢如何有助于补偿在AD脑中观察到的葡萄糖代谢不足。此外,我们提出了CO对认知,β淀粉样蛋白致病性,炎症和氧化应激的神经保护作用的当前证据。本综述探讨了CO / MCFA对其他慢性疾病的影响,这些慢性疾病是AD的危险因素,并解决了文献中关于将CO / MCFA用作AD的潜在治疗方法的空白。
更新日期:2020-01-15
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