A distinct [18F]MPPF PET profile in amnestic mild cognitive impairment compared to mild Alzheimer's disease
A distinct [18F]MPPF PET profile in amnestic mild cognitive impairment compared to mild Alzheimer's disease
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DOI：
10.1016/j.neuroimage.2008.01.030
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发表时间：
2008-04-15
期刊：
影响因子：
5.7
通讯作者：
Krolak-Salmon, P.
中科院分区：
文献类型：
--
作者：
Truchot, L.;Costes, N.;Krolak-Salmon, P.
迄今为止，两项正电子发射断层扫描（PET）研究探讨了5-HT 1A受体密度在阿尔茨海默病（AD）患者的海马。他们显示了这个大脑区域中5-HT 1A受体的早期变化，已知该区域具有密集的多巴胺能神经支配。这些研究仅报告了海马体的测量结果。在目前的PET研究中，我们使用5-HT 1A受体拮抗剂[F-18] MPPF（1）探索与对照人群相比，处于轻度痴呆阶段的AD患者和遗忘型轻度认知障碍（aMCI）患者全脑中的5-HT 1A受体密度;（2）更精确地探讨AD患者和aMCI患者与对照组相比边缘脑区5-HT 1A受体密度。进行基于体素的分析，以评估AD患者和aMCI患者与对照组相比[F-18] MPPF结合潜力（BP）的差异。全脑[F-18] MPPF BP分析显示，AD脑总体降低，而aMCI脑总体升高。在AD脑中，在海马和海马旁回中检测到BP显著降低，而在aMCI脑中在枕下回中观察到BP显著升高。这些全脑结果与先前研究中报告的海马数据一致，显示aMCI组中[F-18] MPPF结合增加，而AD组中[F-18] MPPF结合减少。总之，这些结果表明，在AD阶段这种机制崩溃之前，在aMCI阶段上调α-肾上腺素能代谢说明了代偿机制的含义。α-肾上腺素能受体标记的这种差异允许区分aMCI患者组和轻度AD患者组，每个患者组具有特定的[F-18] MPPF PET谱。(C)2008年由Elsevier Inc.出版
To date, two positron emission tomography ( PET) studies have explored 5-HT1A receptor density in the hippocampus of Alzheimer's disease (AD) patients. They showed early changes of 5-HT1A receptors in this brain region, known to have a dense serotonergic innervation. These studies only reported measurements in hippocampus. In the present PET study, we used an antagonist of 5-HT1A receptors, the [F-18] MPPF (1) to explore 5-HT1A receptor density in the whole brain of AD patients at a mild stage of dementia and amnestic mild cognitive impairment (aMCI) patients compared to a control population; (2) to explore more precisely the 5-HT1A receptor density in the limbic brain regions of AD patients and aMCI patients compared to controls. Voxel-based analyses were performed to assess differences in the [F-18] MPPF binding potential ( BP) between AD patients and aMCI patients compared to controls. Analyses of whole-brain [F-18] MPPF BP showed a global decrease in AD brains in contrast with a global increase in aMCI brains. In AD brains, a significant decrease of BP was detected in hippocampus and parahippocampal gyrus, whereas a significant increase of BP was observed in the inferior occipital gyrus in aMCI brains. These whole brain results are in accordance to hippocampal data reported in a previous study, showing an increase of [F-18] MPPF binding in the aMCI group contrasting with a decrease in the AD group. Altogether, these results suggest the implication of a compensatory mechanism illustrated by an up regulation of serotonergic metabolism at the aMCI stage before a breakdown of this mechanism at the AD stage. This difference of serotonergic receptor labeling allows to distinguish the groups of aMCI patients from mild AD patients with specific [F-18] MPPF PET profiles for each patient group. (C) 2008 Published by Elsevier Inc.