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区域葡萄糖代谢异常并非阿尔茨海默病中萎缩的结果。

Regional glucose metabolic abnormalities are not the result of atrophy in Alzheimer's disease.

作者信息

Ibáñez V, Pietrini P, Alexander G E, Furey M L, Teichberg D, Rajapakse J C, Rapoport S I, Schapiro M B, Horwitz B

机构信息

Laboratory of Neurosciences, National Institute on Aging, National Institutes of Health, Bethesda, MD, USA.

出版信息

Neurology. 1998 Jun;50(6):1585-93. doi: 10.1212/wnl.50.6.1585.

DOI:10.1212/wnl.50.6.1585
PMID:9633698
Abstract

OBJECTIVE

To determine whether the hypometabolism observed in PET images of patients with Alzheimer's disease (AD) is due entirely to brain atrophy.

BACKGROUND

Reduced brain glucose metabolism in AD patients measured using PET has been reported by numerous authors. Actual glucose metabolic values in AD may be reduced artificially because of brain atrophy, which accentuates the partial volume effect (PVE) on data collected by PET.

METHODS

Using segmented MR images, we corrected regional cerebral metabolic rates for glucose for PVEs to evaluate the effect of atrophy on uncorrected values for brain metabolism in AD patients and healthy control subjects.

RESULTS

Global glucose metabolism was reduced significantly before and after correction in AD patients compared with controls. Before PVE correction, glucose metabolic values in patients were lower than in control subjects in the inferior parietal, frontal, and lateral temporal cortex; in the posterior cingulate; and in the precuneus. These reductions remained significantly lower after PVE correction, although in the posterior cingulate the difference in metabolism between AD patients and control subjects lessened. Regional glucose metabolism of these areas with PVE correction was lower in moderately-severely demented patients than in mildly demented patients.

CONCLUSION

Reduced glucose metabolism measured by PET in AD is not simply an artifact due to an increase in CSF space induced by atrophy, but reflects a true metabolic reduction per gram of tissue.

摘要

目的

确定在阿尔茨海默病(AD)患者的正电子发射断层扫描(PET)图像中观察到的代谢减退是否完全归因于脑萎缩。

背景

众多作者报道了使用PET测量的AD患者脑葡萄糖代谢降低。由于脑萎缩会加剧PET收集数据时的部分容积效应(PVE),AD患者的实际葡萄糖代谢值可能会被人为降低。

方法

我们使用分割后的磁共振图像(MR),对葡萄糖的区域脑代谢率进行PVE校正,以评估萎缩对AD患者和健康对照者脑代谢未校正值的影响。

结果

与对照组相比,AD患者在校正前后的整体葡萄糖代谢均显著降低。在PVE校正前,患者在顶下小叶、额叶、颞叶外侧皮质、后扣带回和楔前叶的葡萄糖代谢值低于对照者。尽管在PVE校正后,AD患者和对照者在后扣带回的代谢差异有所减小,但这些区域的代谢降低仍显著低于对照者。校正PVE后,中度至重度痴呆患者这些区域的局部葡萄糖代谢低于轻度痴呆患者。

结论

PET测量的AD患者葡萄糖代谢降低并非仅仅是由于萎缩导致脑脊液空间增加引起的假象,而是反映了每克组织真正的代谢降低。

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