18F stilbenes and styrylpyridines for PET imaging of A beta plaques in Alzheimer's disease: a miniperspective.
18F stilbenes and styrylpyridines for PET imaging of A beta plaques in Alzheimer's disease: a miniperspective.
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DOI：
10.1021/jm901039z
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发表时间：
2010-02-11
影响因子：
7.3
通讯作者：
Skovronsky D
中科院分区：
文献类型：
--
作者：
Kung HF;Choi SR;Qu W;Zhang W;Skovronsky D
阿尔茨海默病（Alzheimer's disease，ADa）是一种以缓慢进行性痴呆为特征的脑神经退行性疾病。这种潜伏的疾病越来越重要，因为它影响了数百万老年患者。AD的临床症状包括认知能力下降、不可逆的记忆丧失、定向障碍和语言障碍。尸检AD脑的主要神经病理学观察结果包括存在含有β-淀粉样蛋白（Aβ）聚集体的老年斑和含有高度磷酸化tau蛋白的神经元缠结（图1A）。1，2一些基因组因素与AD有关。家族性AD（或早发性AD）已被报道在编码β-淀粉样前体蛋白（APP）、早老素1、早老素2和载脂蛋白E（APOE）的基因中具有突变。3导致AD发展的这些突变的确切机制尚不完全清楚;然而，脑中包含Aβ肽的斑块的形成是阿尔茨海默病病理学中的关键事件。大量证据表明，Aβ肽的积聚和聚集可能在AD发病机制中起主要作用。2，4由各种机制产生的Aβ过度负荷可能是神经退行性事件的起点，并可能引发一系列事件（β-淀粉样蛋白级联反应，图1B），包括神经胶质增生、炎症变化、神经炎/突触变化、缠结和递质丢失。2目前，除了通过尸检和脑组织染色来证明Aβ斑块的存在外，还没有明确的方法来诊断AD。最近的报告表明，脑中的β-淀粉样蛋白聚集体在导致AD的一系列事件中起关键作用。2，5因此，开发靶向Aβ聚集体的诊断显像剂在AD的诊断和治疗中非常重要。特异性靶向Aβ斑块的新型PET显像剂可能导致AD的早期检测
Alzheimer’s disease (ADa) is a neurodegenerative disease of the brain characterized by a slowly progressive dementia. This insidious disease is growing in importance because it affects millions of older patients. Clinical symptoms of AD include cognitive decline, irreversible memory loss, disorientation, and language impairment. Major neuropathology observations of post-mortem AD brain include the presence of senile plaques containing β-amyloid (Aβ) aggregates and neurofibrillary tangles containing highly phosphorylated tau proteins (Figure 1A). 1, 2 Several genomic factors have been linked to AD. Familial AD (or early onset AD) has been reported to have mutations in genes encoding β-amyloid precursor protein (APP), presenilin 1, presenilin 2, and apolipoprotein E (APOE). 3 The exact mechanisms of these mutations, which lead to the development of AD, are not fully understood; however, formation of plaques comprising Aβ peptide in the brain is a pivotal event in the pathology of Alzheimer’s disease. Significant evidence suggests that accumulation and aggregation of Aβ peptides may play a major causative role in AD pathogenesis. 2, 4 The excessive burden of Aβ, produced by various mechanisms, may represent the starting point of neurodegenerative events and may initiate a cascade of events (β-amyloid cascade, Figure 1B) that includes gliosis, inflammatory changes, neuritic/synaptic change, tangles, and transmitter loss. 2 Currently, there is no definitive method to diagnose AD except by post-mortem evaluation and staining of the brain tissue, which demonstrates the existence of Aβ plaques.Recent reports have suggested that β-amyloid aggregates in the brain play a key role in a cascade of events leading to AD. 2, 5 Thus, the development of diagnostic imaging agents targeting Aβ aggregates is very important in the diagnosis and treatment of AD. Novel PET imaging agents specifically targeting the Aβ plaques may lead to early detection of AD
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影响因子：
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