中文摘要：

与他们的能力到禁止形成淀粉 -- 肽(A) 纤丝，新肾上素(NE ) ，和另外的儿茶酚衍生物为 Alzheimers 疾病(广告) 的潜在的治疗被考虑了。然而，因为 A 和 NE 的多样的功能，如此的处理在广告病理仍然保持可争辩。而且，伴随 NE 的复杂氧化引起了以前的研究的多数集中于 NE 氧化物的绑定到 A 上。A 与 NE 的减小状态由交往的分子的机制，与大脑功能被相关，应该着急地被探索。在这个工作，由控制严密厌氧的试验性的条件， A/NE 相互作用的分子的机制被调查，并且二个有约束力的地点被揭示。因为 NE 的强壮的有约束力的地点，和 SNK (26-28 ) 片断是弱有约束力的片断， Tyr ¹⁰ 被识别。而且， thioflavin T 荧光证实了与 SNK (26-28 ) 片断通过它的弱绑定禁止聚集的 NE 积极功能。同时， 7-OHCCA 荧光展出了 NE 提高的否定功能 ? 睳慥'S 湡吗？

英文摘要：

With their capability to inhibit the formation of amyloid-p peptide （Aβ） fibril, norepinephrine （NE）, and other catechol derivatives have been considered for the potential treatment of Alzheimer＇s disease （AD）. Such treatment, however, remains debatable because of the diverse functions of Aβ and NE in AD pathology. Moreover, the complicated oxidation accompanying NE has caused the majority of the previous research to focus on the binding of NE oxides onto Aβ. The molecular mechanism by which Aβ interacts with the reduction state of NE, which is correlated with the brain function, should be urgently explored. In this work, by controlling rigorous anaerobic experimen- tal conditions, the molecular mechanism of the Aβ/NE interaction was investigated, and two bind- ing sites were revealed. Tyr10 was identified as the strong binding site of NE, and SNK（26-28） segment was the weak binding segment. Furthermore, thioflavin T fluorescence confirmed NE＇s positive function of inhibiting Aβ aggregation through its weak binding with SNK（26-28） segment. Meanwhile, 7-OHCCA fluorescence exhibited NE＇s negative function of enhancing .OH generation through inhibiting the Aβ/Cu2＋ coordination. The viability tests of the neuroblastoma SH-SY5Y cells displayed that the coexistence of NE, Cu2＋, and Aβ induced lower cell viability than free Cu2＋, indicating the significant negative effect of excessive NE on AD progression. These data revealed the possible pathway of NE-induced damage in AD brain, which is significant for understanding the function of NE in Aβ-involved AD neuropathology and for designing an NE-related therapeutic strategy for AD.