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Vascular dysfunction in Alzheimer’s disease: a biomarker of disease progression and a potential therapeutic target

机译：阿尔茨海默病的血管功能障碍：疾病进展的生物标志物和潜在的治疗目标

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Alzheimer’s disease (AD) is a progressive neurodegenerative disorder and the predominant form of dementia. Since its initial description by Alois Alzheimer in 1906, several advances have been made in our understanding of the progression of the disease and its clinical consequences, yet the underlying etiology remains contentious. Given the stereotyped patterns of cortical and hippocampal neuronal loss and the progressive degeneration of key neurotransmitter pathways, research has traditionally been focused on factors affecting neuronal viability, including the contribution of glial dysfunction to neuronal degeneration. From a clinical perspective, the fruits of this work have been underwhelming. Key pathological markers of the disease, including β-amyloid (Aβ) plaque formation and tau hyperphosphorylation, have yielded no effective therapies, highlighted by the recent discontinuations of several high profile Aβ immunotherapy trials. The few current symptomatic therapies for AD are predicated on the amelioration of cholinergic or glutamatergic dysfunction. Aside from underscoring the inadequacy of current therapeutic approaches, this also points to the importance of alternative contributors to AD pathogenesis. In recent years, there has been a growing appreciation for the multimodal and multifactorial nature of the condition; the case for combinatorial therapies is thus strong.
机译：阿尔茨海默病（AD）是一种渐进神经退行性疾病和痴呆的主要形式。自1906年的Alois Alzheimer初次描述以来，我们对疾病进展的了解及其临床后果的几个进步，但潜在的病因仍然有争议。鉴于皮质和海马神经元丧失的刻板印象模式和关键神经递质途径的进步退化，传统上传统上专注于影响神经元活力的因素，包括胶质功能障碍对神经元变性的贡献。从临床的角度来看，这项工作的成果一直是强大的。疾病的关键病理标志物，包括β-淀粉样（Aβ）斑块形成和Tau超磷酸化，没有得到有效的疗法，通过最近几种高型Aβ免疫治疗试验的最近停止突出。少数目前的AD症状疗法旨在改善胆碱能或谷氨酸功能障碍的改善。除了强调当前治疗方法的不足之处，这还指出了替代贡献者对AD发病机制的重要性。近年来，对病情的多式联运和多重情绪性质越来越高兴;因此，组合疗法的情况强大。

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