据澳大利亚“新快网”3月20日报道，墨尔本研究人员认为蛇毒可能可以治疗引起阿尔茨海默氏病的神经斑，提出预防阿尔茨海默氏病新疗法。 

　　据报道，莫纳什大学科研人员发现，美国南部及中部某种响尾蛇的毒液可以破坏淀粉样蛋白，而这种物质是引发阿尔茨海默氏病的原因。 

　　健康人的生物酶可以分解淀粉样蛋白，但是阿尔茨海默氏病患者生物酶停止工作，使得淀粉样蛋白累计，最终导致斑块沉积而造成严重后果。 

　　阿尔茨海默氏病及痴呆症相关疾病影响澳大利亚35万人生活，每年耗费卫生及老年人护理系统50亿澳元资金。 

　　研究人员一直在寻找激活生物酶，以继续分解淀粉样蛋白的物质。莫纳什研究员桑佳亚(Sanjaya Kuruppu)及莫纳什大学生物医疗研究机构(Biomedicine Discovery Institute)史密斯(Ian Smith)教授认为他们终于找到答案。 

　　他们的研究结果发表在了杂志《自然》系列《科学报告》(Scientific Reports)上。（来源：环球网） 

　　N-terminal domain of Bothrops asper Myotoxin II Enhances the Activity of Endothelin Converting Enzyme-1 and Neprilysin 

　　Abstract  Neprilysin (NEP) and endothelin converting enzyme-1 (ECE-1) are two enzymes that degrade amyloid beta in the brain. Currently there are no molecules to stimulate the activity of these enzymes. Here we report, the discovery and characterisation of a peptide referred to as K49-P1-20, from the venom of Bothrops asper which directly enhances the activity of both ECE-1 and NEP. This is evidenced by a 2- and 5-fold increase in the Vmax of ECE-1 and NEP respectively. The K49-P1-20 concentration required to achieve 50% of maximal stimulation (AC50) of ECE-1 and NEP was 1.92 ± 0.07 and 1.33 ± 0.12 μM respectively. Using BLITZ biolayer interferometry we have shown that K49-P1-20 interacts directly with each enzyme. Intrinsic fluorescence of the enzymes change in the presence of K49-P1-20 suggesting a change in conformation. ECE-1 mediated reduction in the level of endogenous soluble amyloid beta 42 in cerebrospinal fluid is significantly higher in the presence of K49-P1-20 (31 ± 4% of initial) compared with enzyme alone (11 ± 5% of initial; N = 8, P = 0.005, unpaired t-test). K49-P1-20 could be an excellent research tool to study mechanism(s) of enzyme stimulation, and a potential novel drug lead in the fight against Alzheimer’s disease.