在阿尔茨海默病中，β-淀粉样蛋白的积累是一种最终失败的保护机制。
In Alzheimer's disease, amyloid beta accumulation is a protective mechanism that ultimately fails.
作者信息
Rischel Elise Brøchner, Gejl Michael, Brock Birgitte, Rungby Jørgen, Gjedde Albert
机构信息
Department of Neuroscience, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.
Department of Biomedicine, Aarhus University, Aarhus, Denmark.
出版信息
Alzheimers Dement. 2023 Mar;19(3):771-783. doi: 10.1002/alz.12701. Epub 2022 Jun 8.
HYPOTHESIS AND PREDICTIONS
Here, we claim that amyloid beta (Aβ) accumulation is a protective mechanism that ultimately fails. We predict that more Aβ accumulates in regions with higher rates of glucose metabolism, reaching a maximum followed by progression of pathology.
BACKGROUND
Aβ accumulation is characteristic of Alzheimer's disease (AD) but the accumulation does not correlate with cognitive decline, unlike the rates of glucose metabolism.
STRATEGY
We compared averaged and individual estimates of regional binding potentials of [C]Pittsburgh compound B to regionally averaged and individual values of metabolism of [F]fluorodeoxyglucose in brain regions of volunteers with AD.
SIGNIFICANCE
The claim explains the cognitive decline in some patients at a significantly lower level of Aβ deposition than in other patients, as well as the presence of cognitively healthy individuals with high Aβ accumulation. With further support of the hypothesis, the significance of Aβ accumulation in brains of patients with AD may require revision.
假说与预测
在此，我们认为β淀粉样蛋白（Aβ）的积累是一种最终失效的保护机制。我们预测，在葡萄糖代谢率较高的区域会积累更多的Aβ，达到最大值后随病理学进展而变化。
背景
Aβ积累是阿尔茨海默病（AD）的特征，但与葡萄糖代谢率不同，这种积累与认知衰退并无关联。
策略
我们将[C]匹兹堡化合物B区域结合电位的平均估计值和个体估计值，与患有AD的志愿者脑区中[F]氟脱氧葡萄糖代谢的区域平均值和个体值进行了比较。
意义
该假说解释了一些患者在Aβ沉积水平显著低于其他患者时出现认知衰退的现象，以及存在Aβ积累量高但认知健康的个体。随着该假说得到进一步支持，AD患者大脑中Aβ积累的意义可能需要修正。
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