近日，来自英国基尔大学的研究者通过研究揭示，铜不仅仅可以帮助个体的大脑抵御β-淀粉样蛋白形成这折叠片，而且铜也直接参与了阿尔兹海默症患者大脑中衰老斑的形成。
研究揭示，大脑中低水平的铜可以促进某种特定机制的发生，这种机制就是在阿尔兹海默症疾病中，β淀粉样蛋白可以以衰老斑的形式存在。
目前研究者研究的重点就是调查是否大脑中的铜可以促使阿尔兹海默症患者大脑中衰老斑的形成，此前研究中，研究者指出，铜的存在可以保护β淀粉样蛋白免于聚集形成折叠片以及形成衰老斑，当然研究者希望通过后期的深入研究来阐明其中所发生的分子机理医`学教育网搜集整理。
该项研究以“Copper prevents amyloid-β1-42 from forming amyloid fibrils under near-physiological conditions in vitro”为题刊登于国际著名杂志杂志Nature的子刊Scientific Reports上。
The aggregation and deposition of amyloid-β（1–42） （Aβ42） in the brain is implicated in the aetiology of Alzheimer's disease （AD）。 While the mechanism underlying its deposition in vivo is unknown its precipitation in vitro is influenced by metal ions. For example， Aβ42 is known to bind copper， Cu（II）， in vitro and binding results in aggregation of the peptide. The biophysical properties of Cu（II）-Aβ42 aggregates are of significant importance to their putative involvement in the amyloid cascade hypothesis of AD and are currently the subject of strong debate. In particular the question has been raised if sub- and super-stoichiometric concentrations of Cu（II） act in opposing ways in respectively accelerating and preventing amyloid fibril formation by Aβ42. Herein we have used fluorimetry and transmission electron microscopy to provide unequivocal evidence that under near-physiological conditions both sub- and super-stoichiometric concentrations of Cu（II） prevented the assembly of Aβ4
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