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评估作为家畜饲料添加剂的莱克多巴胺在肉类中的残留对阿尔茨海默病的潜在影响。

Assessing the Possible Influence of Residues of Ractopamine, a Livestock Feed Additive, in Meat on Alzheimer Disease.

作者信息

Fan Frank S

机构信息

Section of Hematology and Oncology, Department of Medicine, Ministry of Health and Welfare Taitung Hospital, Taitung, Taiwan.

出版信息

Dement Geriatr Cogn Dis Extra. 2021 May 7;11(2):110-113. doi: 10.1159/000515677. eCollection 2021 May-Aug.

Abstract

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 Alz-heimer 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.

摘要

饲料添加剂莱克多巴胺是一种β-肾上腺素能激动剂,已被批准用于家畜近20年。过去,关于其对人类可能的不良影响的研究仅集中在心血管疾病和心血管功能障碍方面。在本文中,将基于最近有争议的研究结果进行讨论,即β-肾上腺素能受体激活不仅能刺激阿尔茨海默病致病的淀粉样蛋白-β积累,而且在独立的实验室研究中还能增强海马神经发生并改善小鼠记忆缺陷,探讨莱克多巴胺是否以及如何影响神经退行性变,无论是促进还是降低阿尔茨海默病的发病率。此外,已发现环境富集可预防与记忆相关的海马长时程增强的损害以及由淀粉样蛋白-β诱导的小胶质细胞介导的神经炎症。这些有益作用主要通过增强β-肾上腺素能信号传导实现,并且可以被β激动剂异丙肾上腺素模拟。最后,已证明β-肾上腺素能激动剂沙丁胺醇可直接与tau蛋白结合,并干扰在阿尔茨海默病前驱期所见的tau丝形成。这些复杂但有趣的问题导致了关于肉类中莱克多巴胺残留对阿尔茨海默病可能影响的相互矛盾的推测。本综述得出的假设在未来肯定值得精心设计的实验室研究和临床研究。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/00f3/8215976/681e1525bac8/dee-0011-0110-g01.jpg

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