Department of Geriatrics, Center for Aging Brain, Memory Unit, University of Bari, Policlinico, Piazza Giulio Cesare, 11, 70124 Bari, Italy.
Ageing Res Rev. 2010 Apr;9(2):184-99. doi: 10.1016/j.arr.2009.07.005. Epub 2009 Jul 28.
Drugs currently used in the treatment of cognitive impairment and dementia have a very limited therapeutic value, suggesting the necessity to potentially individualize new strategies able to prevent and to slow down the progression of predementia and dementia syndromes. An increasing body of epidemiological evidence suggested that elevated saturated fatty acids (SFA) could have negative effects on age-related cognitive decline (ARCD) and mild cognitive impairment (MCI). Furthermore, a clear reduction of risk for cognitive decline has been found in population samples with elevated fish consumption, high intake of monounsaturated fatty acids (MUFA) and polyunsaturated fatty acids (PUFA), particularly n-3 PUFA. Epidemiological findings demonstrated that high PUFA intake appeared to have borderline non-significant trend for a protective effect against the development of MCI. Several hypotheses could explain the association between dietary unsaturated fatty acids and cognitive functioning, including mechanisms through the co-presence of antioxidant compounds in food groups rich in fatty acids, via atherosclerosis and thrombosis, inflammation, accumulation of b-amyloid, or via an effect in maintaining the structural integrity of neuronal membranes, determining the fluidity of synaptosomal membranes that thereby regulate neuronal transmission. However, recent findings from clinical trials with n-3 PUFA supplementation showed efficacy on depressive symptoms only in non-apolipoprotein E (APOE) epsilon4 carriers, and on cognitive symptoms only in very mild Alzheimer's disease (AD) subgroups, MCI patients, and cognitively unimpaired subjects non-APOE epsilon4 carriers. These data together with epidemiological evidence support a possible role of fatty acid intake in maintaining adequate cognitive functioning and possibly for the prevention and management of cognitive decline and dementia, but not when the AD process has already taken over.
目前用于治疗认知障碍和痴呆的药物的治疗价值非常有限，这表明有必要制定新的策略，以潜在地针对每个患者进行个体化治疗，从而预防和减缓前驱期痴呆和痴呆综合征的进展。越来越多的流行病学证据表明，升高的饱和脂肪酸（SFA）可能对与年龄相关的认知衰退（ARCD）和轻度认知障碍（MCI）产生负面影响。此外，在鱼类摄入量高、单不饱和脂肪酸（MUFA）和多不饱和脂肪酸（PUFA）摄入量高的人群样本中，发现认知能力下降的风险明显降低，特别是 n-3 PUFA。流行病学研究结果表明，高 PUFA 摄入量似乎对预防 MCI 的发展具有保护作用，但呈临界非显著性趋势。有几种假说可以解释膳食不饱和脂肪酸与认知功能之间的关系，包括通过富含脂肪酸的食物组中抗氧化化合物的共同存在、通过动脉粥样硬化和血栓形成、炎症、β-淀粉样蛋白的积累，或通过维持神经元膜结构完整性的机制，从而调节神经元传递。然而，最近 n-3 PUFA 补充临床试验的结果表明，n-3 PUFA 补充剂仅对非载脂蛋白 E（APOE）ε4 携带者的抑郁症状有效，仅对非常轻度的阿尔茨海默病（AD）亚组、MCI 患者和认知正常的非 APOE ε4 携带者的认知症状有效。这些数据以及流行病学证据支持脂肪酸摄入在维持适当的认知功能以及预防和管理认知能力下降和痴呆方面可能发挥作用，但前提是 AD 进程尚未发生。
