Department of Psychiatry and Neurochemistry, Clinical Neurochemistry Laboratory, Institute of Neuroscience and Physiology, the Sahlgrenska Academy at the University of Gothenburg, S-431 80 Mölndal, Sweden.
Expert Rev Neurother. 2014 Jun;14(6):621-30. doi: 10.1586/14737175.2014.915740.
The increasing prevalence of Alzheimer's disease (AD) and a lack of effective prevention or disease-modifying therapies are global challenges with devastating personal, social and economic consequences. The amyloid β (Aβ) hypothesis posits that cerebral β-amyloidosis is a critical early event in AD pathogenesis. However, failed clinical trials of Aβ-centric drug candidates have called this hypothesis into question. Whereas we acknowledge that the Aβ hypothesis is far from disproven, we here re-visit the links between Aβ, tau and neurodegeneration. We review the genetics, epidemiology and pathology of sporadic AD and give an updated account of what is currently known about the molecular pathogenesis of the disease.
阿尔茨海默病（AD）的发病率不断上升，而有效的预防或疾病修饰疗法却缺乏，这是一个具有全球挑战性的问题，给个人、社会和经济带来了灾难性的后果。β-淀粉样蛋白（Aβ）假说认为，脑β-淀粉样蛋白病是 AD 发病机制中的一个关键早期事件。然而，以 Aβ 为中心的药物候选物的临床试验失败，使这一假说受到质疑。虽然我们承认 Aβ 假说还远未被否定，但我们在这里重新审视 Aβ、tau 和神经退行性变之间的联系。我们回顾了散发性 AD 的遗传学、流行病学和病理学，并更新了目前对该疾病分子发病机制的了解。
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