Department of Medical Biochemistry and Immunology, School of Medicine, Cardiff University, Heath Park, Cardiff, UK.
J Cell Mol Med. 2009 Nov-Dec;13(11-12):4329-48. doi: 10.1111/j.1582-4934.2009.00889.x. Epub 2009 Sep 1.
Alzheimer's disease (AD) is an age-related neurodegenerative disease that affects approximately 24 million people worldwide. A number of different risk factors have been implicated in AD; however, neuritic (amyloid) plaques are considered as one of the defining risk factors and pathological hallmarks of the disease. In the past decade, enormous efforts have been devoted to understand the genetics and molecular pathogenesis leading to neuronal death in AD, which has been transferred into extensive experimental approaches aimed at reversing disease progression. Modern medicine is facing an increasing number of treatments available for vascular and neurodegenerative brain diseases, but no causal or neuroprotective treatment has yet been established. Almost all neurological conditions are characterized by progressive neuronal dysfunction, which, regardless of the pathogenetic mechanism, finally leads to neuronal death. The particular emphasis of this review is on risk factors and mechanisms resulting in neuronal loss in AD and current and prospective opportunities for therapeutic interventions. This review discusses these issues with a view to inspiring the development of new agents that could be useful for the treatment of AD.
阿尔茨海默病（AD）是一种与年龄相关的神经退行性疾病，影响全球约 2400 万人。许多不同的风险因素与 AD 有关；然而，神经突（淀粉样）斑块被认为是该疾病的一个重要的风险因素和病理标志物。在过去的十年中，人们投入了大量的努力来了解导致 AD 神经元死亡的遗传学和分子发病机制，这已转化为广泛的旨在逆转疾病进展的实验方法。现代医学面临着越来越多的血管和神经退行性脑疾病的治疗方法，但尚未建立任何因果或神经保护治疗方法。几乎所有的神经疾病都以进行性神经元功能障碍为特征，无论发病机制如何，最终都会导致神经元死亡。这篇综述的特别重点是导致 AD 神经元丧失的风险因素和机制，以及目前和未来的治疗干预机会。本文综述了这些问题，以期激发开发新的药物，这些药物可能对 AD 的治疗有用。
