Membrane interactions and neurotoxicity of Amyloid Abeta peptides from Alzheimer's disease.

人类寿命延长的一个结果是与年龄相关的神经退行性疾病，如阿尔茨海默病(AD)更加普遍。目前，阿尔茨海默病的治疗方法有限，没有治愈的方法。导致阿尔茨海默病的关键蛋白是Abeta，这种多肽的毒性物种的特征对于确定潜在的治疗靶点至关重要。这项建议旨在研究人工合成的突变多肽，并确定膜结合位点。通过确定哪些脂质与Abeta的膜结合以及随后的细胞死亡起关键作用，可以开发药物来阻止Abeta与膜的结合，从而导致神经元存活和防止AD患者的记忆丧失。

A consequence of the increase in human life span is that age-related neurodegenerative diseases such as Alzheimer's disease (AD) are more prevalent. Currently there are limited therapeutic treatments and no cure for AD. The key protein causing AD is Abeta and characterization of the toxic species of this peptide is critical towards identifying potential therapeutic targets. This proposal aims to study mutant peptides made synthetically and to identify a membrane-binding site. By establishing which lipid is critically involved in membrane binding of Abeta and mediating subsequent cell death, drugs may be developed to prevent the binding of Abeta to membranes resulting in neuronal survival and prevention of memory loss in AD patients.