Istituto di Biomedicina ed Immunologia Molecolare (IBIM), CNR, Palermo, Italy.
J Phys Condens Matter. 2012 Jun 20;24(24):244102. doi: 10.1088/0953-8984/24/24/244102. Epub 2012 May 18.
Alzheimer's disease (AD) is the most common form of dementia among older people. Dementia is an irreversible brain disorder that seriously affects a person's ability to carry out daily activities. It is characterized by loss of cognitive functioning and behavioral abilities, to such an extent that it interferes with the daily life and activities of the affected patients. Although it is still unknown how the disease process begins, it seems that brain damage starts a decade or more before problems become evident. Scientific data seem to indicate that changes in the generation or the degradation of the amyloid-b peptide (Aβ) lead to the formation of aggregated structures that are the triggering molecular events in the pathogenic cascade of AD. This review summarizes some characteristic features of Aβ misfolding and aggregation and how cell damage and death mechanisms are induced by these supramolecular and toxic structures. Further, some interventions for the early diagnosis of AD are described and in the last part the potential therapeutic strategies adoptable to slow down, or better block, the progression of the pathology are reported.
阿尔茨海默病（AD）是老年人中最常见的痴呆症形式。痴呆症是一种不可逆的大脑疾病，严重影响患者进行日常活动的能力。其特征是认知功能和行为能力丧失，以至于严重影响到受影响患者的日常生活和活动。尽管目前尚不清楚疾病过程是如何开始的，但似乎大脑损伤在出现问题的十年甚至更早之前就开始了。科学数据似乎表明，淀粉样蛋白-β肽（Aβ）的产生或降解的变化导致聚集结构的形成，这些聚集结构是 AD 发病级联反应中的触发分子事件。本综述总结了 Aβ错误折叠和聚集的一些特征，以及这些超分子和毒性结构如何诱导细胞损伤和死亡机制。此外，还描述了一些用于 AD 早期诊断的干预措施，最后一部分报告了可采用的减缓或更好地阻止该病理学进展的潜在治疗策略。
