Delobette S, Privat A, Maurice T
I.N.S.E.R.M. Unité 336, Ecole Nationale Supérieure de Chimie, Montpellier, France.
Eur J Pharmacol. 1997 Jan 14;319(1):1-4. doi: 10.1016/s0014-2999(96)00922-3.
The beta-amyloid peptide-(25-35) fragment, but not beta-amyloid peptide-(1-28), shares with beta-amyloid protein-(1-42) the ability to self-aggregate and to induce neurotoxicity in vitro. This study examined the induction of amnesia in rats given intracerebroventricularly soluble or aggregated beta-amyloid peptide-(25-35) (5-45 nmol), or beta-amyloid peptide-(1-28) (15 nmol). Memory deficit in the water-maze test, examined 14 days after aggregated beta-amyloid peptide-(25-35) injection, was more pronounced than with soluble beta-amyloid peptide-(25-35). beta-Amyloid peptide-(1-28) only affected retention. These results confirm the direct amnesic properties of beta-amyloid peptides in the rat brain and showed that prior peptide aggregation markedly facilitates the appearance of amnesia.
β-淀粉样肽-（25-35）片段，而非β-淀粉样肽-（1-28），与β-淀粉样蛋白-（1-42）一样，具有体外自我聚集和诱导神经毒性的能力。本研究检测了向大鼠脑室内注射可溶性或聚集态的β-淀粉样肽-（25-35）（5-45纳摩尔）或β-淀粉样肽-（1-28）（15纳摩尔）后对大鼠失忆的诱导情况。在注射聚集态β-淀粉样肽-（25-35）14天后进行的水迷宫试验中，记忆缺陷比注射可溶性β-淀粉样肽-（25-35）时更明显。β-淀粉样肽-（1-28）仅影响记忆保持。这些结果证实了β-淀粉样肽在大鼠脑中具有直接导致失忆的特性，并表明肽的预先聚集显著促进了失忆的出现。
