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Assessing the Possible Influence of Residues of Ractopamine, a Livestock Feed Additive, in Meat on Alzheimer Disease
Dementia and Geriatric Cognitive Disorders Extra ( IF 1.4 ) Pub Date : 2021-05-07 , DOI: 10.1159/000515677
Frank S. Fan

The feed additive ractopamine, a β-adrenergic agonist, has been approved for use in livestock for nearly 2 decades. Studies of its possible adverse effects in humans have concentrated exclusively on cardiovascular disease and cardiovascular functional disorders in the past. In this article, whether and how ractopamine may affect neurodegeneration, either to promote or to reduce the incidence of Alz­heimer disease, will be discussed based on the recent controversial findings that β-adrenoreceptor activation not only can stimulate Alzheimer-pathogenic amyloid-β accumulation but also are able to enhance hippocampal neurogenesis and ameliorate mouse memory deficits in independent laboratory studies. Furthermore, environmental enrichment has been found to prevent impairment of memory-related hippocampal long-term potentiation and microglia-mediated neuroinflammation induced by amyloid-β. These beneficial effects are achieved mainly through enhanced β-adrenergic signaling and can be imitated by β agonist isoprotenerol. Finally, it has been demonstrated that the β-adrenergic agonist salbutamol could bind directly to tau protein and interfere with the tau filament formation seen in the prodromal phase of Alzheimer disease. These complex but interesting issues lead to contradictory speculations of possible effects of ractopamine residue in meat on Alzheimer disease. Hypotheses derived from this review surely deserve carefully designed laboratory investigations and clinical studies in the future.
Dement Geriatr Cogn Disord Extra 2021;11:110–113


中文翻译:

评估肉中莱克多巴胺(一种牲畜饲料添加剂)的残留物对阿尔茨海默病的可能影响

饲料添加剂莱克多巴胺(一种β-肾上腺素能激动剂)已被批准用于牲畜已有近二十年的历史。过去,对人类可能产生的不良影响的研究仅集中于心血管疾病和心血管功能障碍。在这篇文章中,将基于最近有争议的研究结果来讨论莱克多巴胺是否以及如何影响神经变性,从而促进或减少阿尔茨海默氏病的发生,β-肾上腺素受体的活化不仅可以刺激阿尔茨海默氏病致病性淀粉样蛋白β的积累,而且可以在独立的实验室研究中,它们还能够增强海马神经发生并改善小鼠的记忆缺陷。此外,已发现环境富集可防止淀粉样蛋白-β诱导的记忆相关海马长时程增强和小胶质细胞介导的神经炎症损害。这些有益作用主要是通过增强的β-肾上腺素信号传导来实现的,并且可以被β激动剂异戊烯醇所模仿。最后,已经证明,β-肾上腺素能激动剂沙丁胺醇可以直接结合到tau蛋白上,并干扰在阿尔茨海默氏病前驱期所见的tau细丝形成。这些复杂但有趣的问题导致人们对肉中莱克多巴胺残留物对阿尔茨海默氏病的可能影响产生了相互矛盾的推测。从这次审查得出的假设肯定值得在将来进行精心设计的实验室研究和临床研究。这些有益作用主要是通过增强的β-肾上腺素信号传导来实现的,并且可以被β激动剂异戊烯醇所模仿。最后,已经证明,β-肾上腺素能激动剂沙丁胺醇可以直接结合到tau蛋白上,并干扰在阿尔茨海默氏病前驱期所见的tau细丝形成。这些复杂但有趣的问题导致人们对肉中莱克多巴胺残留物对阿尔茨海默氏病的可能影响产生了相互矛盾的推测。从这次审查得出的假设肯定值得在将来进行精心设计的实验室研究和临床研究。这些有益作用主要是通过增强的β-肾上腺素信号传导来实现的,并且可以被β激动剂异戊烯醇所模仿。最后,已经证明β-肾上腺素能激动剂沙丁胺醇可以直接与tau蛋白结合并干扰在阿尔茨海默氏病前驱期所见的tau细丝形成。这些复杂但有趣的问题导致人们对肉中莱克多巴胺残留物对阿尔茨海默氏病的可能影响产生了相互矛盾的推测。从这次审查得出的假设肯定值得在将来进行精心设计的实验室研究和临床研究。已经证明,β-肾上腺素能激动剂沙丁胺醇可以直接与tau蛋白结合,并干扰阿尔茨海默氏病前驱期所见的tau细丝形成。这些复杂但有趣的问题导致人们对肉中莱克多巴胺残留物对阿尔茨海默氏病的可能影响产生了相互矛盾的推测。从这次审查得出的假设肯定值得在将来进行精心设计的实验室研究和临床研究。已经证明,β-肾上腺素能激动剂沙丁胺醇可以直接与tau蛋白结合,并干扰阿尔茨海默氏病前驱期所见的tau细丝形成。这些复杂但有趣的问题导致人们对肉中莱克多巴胺残留物对阿尔茨海默氏病的可能影响产生了相互矛盾的推测。从这次审查得出的假设肯定值得在将来进行精心设计的实验室研究和临床研究。
Dement Geriatr Cogn Disord Extra 2021; 11:110–113
更新日期:2021-05-07
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