Pahnke J, Krohn M, Scheffler K
Universität Rostock, Klinik und Poliklinik für Neurologie, Neurodegeneration Research Lab, Gehlsheimer Strasse 20, Rostock.
Fortschr Neurol Psychiatr. 2009 Aug;77 Suppl 1:S21-4. doi: 10.1055/s-0028-1109601. Epub 2009 Aug 14.
Alzheimer's disease (AD) is a devastating neurodegenerative disorder affecting more than 27 million people worldwide and leading to severe social-economic problems. One characteristic hallmark of AD--the amyloid plaques--are still being discussed to be one important triggering factor. However, current animal and autopsy studies refer to soluble and highly toxic A block oligomers as the deadly agent for the neurons. Current therapies mainly rely on the abatement of symptoms without antagonizing the etiology of the disease. Potential new approaches address reduced production, increased degradation and/or evacuation of toxic A block peptides from the brain. Among others one important group of target-proteins are the ABC transporters of the blood-brain barrier which contribute importantly to the detoxification of the brain. Changes of specific transport functions evoke important alterations for the known pathogenesis and future therapies of AD, especially approaches that target plaque dissolution and plaque reduction.
阿尔茨海默病(AD)是一种毁灭性的神经退行性疾病,全球有超过2700万人受其影响,并导致严重的社会经济问题。AD的一个特征性标志——淀粉样斑块——仍被认为是一个重要的触发因素。然而,目前的动物和尸检研究表明,可溶性且剧毒的Aβ寡聚体才是神经元的致命因素。目前的治疗主要依赖于缓解症状,而没有对抗疾病的病因。潜在的新方法包括减少有毒Aβ肽的产生、增加其降解和/或从大脑中清除。其中一个重要的靶蛋白组是血脑屏障的ABC转运蛋白,它们对大脑的解毒起着重要作用。特定转运功能的变化会引起AD已知发病机制和未来治疗的重要改变,尤其是针对斑块溶解和减少斑块的方法。