Aprahamian Ivan, Stella Florindo, Forlenza Orestes V
Laboratory of Neuroscience (LIM 27) Department & Institute of Psychiatry, Faculty of Medicine,University of São Paulo, Brazil.
Indian J Med Res. 2013 Oct;138(4):449-60.
Alzheimer's disease (AD) is a progressive and irreversible neurodegenerative disease, and corresponds to the most common cause of dementia worldwide. Although not fully understood, the pathophysiology of AD is largely represented by the neurotoxic events triggered by the beta-amyloid cascade and by cytoskeletal abnormalities subsequent to the hyperphosphorylation of microtubule-associated Tau protein in neurons. These processes lead respectively to the formation of neuritic plaques and neurofibrillary tangles, which are the pathological hallmarks of the disease. Clinical benefits of the available pharmacological treatment for AD with antidementia drugs (namely cholinesterase inhibitors and memantine) are unquestionable, although limited to a temporary, symptomatic support to cognitive and related functions. Over the past decade, substantial funding and research have been dedicated to the search and development of new pharmaceutical compounds with disease-modifying properties. The rationale of such approach is that by tackling key pathological processes in AD it may be possible to attenuate or even change its natural history. In the present review, we summarize the available evidence on the new therapeutic approaches that target amyloid and Tau pathology in AD, focusing on pharmaceutical compounds undergoing phase 2 and phase 3 randomized controlled trials.
阿尔茨海默病(AD)是一种进行性且不可逆的神经退行性疾病,是全球范围内痴呆最常见的病因。尽管尚未完全明确,但AD的病理生理学主要表现为β-淀粉样蛋白级联反应引发的神经毒性事件,以及神经元中微管相关Tau蛋白过度磷酸化后导致的细胞骨架异常。这些过程分别导致神经炎性斑块和神经原纤维缠结的形成,它们是该疾病的病理标志。抗痴呆药物(即胆碱酯酶抑制剂和美金刚)对AD进行药物治疗的临床益处是毋庸置疑的,尽管仅限于对认知及相关功能的临时对症支持。在过去十年中,大量资金和研究致力于寻找和开发具有疾病修饰特性的新药物化合物。这种方法的基本原理是,通过解决AD中的关键病理过程,有可能减弱甚至改变其自然病程。在本综述中,我们总结了针对AD中淀粉样蛋白和Tau病理的新治疗方法的现有证据,重点关注正在进行2期和3期随机对照试验的药物化合物。