Mapping brain beta-amyloid.
Mapping brain beta-amyloid.
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DOI：
10.1097/wco.0b013e32832d93c7
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发表时间：
2009-08
影响因子：
4.8
通讯作者：
Jagust W
中科院分区：
文献类型：
--
作者：
Jagust W
本文回顾了使用正电子发射断层扫描 (PET) 进行淀粉样蛋白成像领域的最新进展，特别是量化大脑 Aβ 数量和分布的能力，这种蛋白质在阿尔茨海默病 (AD) 发病机制的主要理论中占据着核心地位。一些影像病理学相关性通过显示 Aβ 沉积的体内测量和组织学测量之间良好的一致性，使该技术本身奠定了更坚实的基础。 Aβ 与其他痴呆症指标（认知、脑萎缩和葡萄糖代谢）之间的相关性似乎支持这样一种观点，即 Aβ 会引发一系列与痴呆症严重程度和进展密切相关的下游变化。然而，β-淀粉样蛋白的 PET 测量与认知之间的关联通常相当弱。对临床使用的影响仍不确定。淀粉样蛋白成像可能有助于区分与 Aβ 相关的痴呆和非 Aβ 相关的痴呆，但这种方法的实用性将取决于有效的 Aβ 导向治疗的可用性。同样，淀粉样蛋白成像有可能预测哪些非痴呆个体最终会患上 AD，尽管下游 Aβ 效应的测量可能很重要。量化大脑中 Aβ 病理学的发生和进展的能力为研究有关个体和神经脆弱性以及 AD 本身的淀粉样蛋白假说的一系列问题提供了潜力。这些发现将具有重要的基础和临床意义。
This article reviews recent developments in the field of amyloid imaging using positron emission tomography (PET), specifically the ability to quantify the amount and distribution of brain Aβ, the protein that occupies a central position in leading theories of the pathogenesis of Alzheimer's disease (AD). Several imaging-pathology correlations place the technique itself on a stronger footing by showing good agreement between in vivo and histological measures of Aβ deposition. Correlations between Aβ and other measures of dementia – cognition, brain atrophy, and glucose metabolism – appear to support a view that Aβ triggers a host of downstream alterations that are closely related to dementia severity and progression. However, associations between PET measures of β-amyloid and cognition are generally fairly weak. The implications for clinical use are still uncertain. It seems likely that amyloid imaging will be useful for differentiating dementias associated with Aβ from those that are not, but the utility of this approach will depend on the availability of effective Aβ-directed treatments. Similarly, amyloid imaging offers the potential for predicting which non-demented individuals will eventually develop AD although here again the measurement of downstream Aβ effects may be important. The ability to quantify the onset and progression of Aβ pathology in the brain offers the potential for investigating a host of questions concerning individual and neural vulnerability and the amyloid hypothesis of AD itself. These findings will have important basic and clinical implications.