LENITEM Laboratory of Epidemiology, Neuroimaging and Telemedicine, IRCCS S. Giovanni di Dio-Fatebenefratelli, Brescia, Italy.
Dement Geriatr Cogn Disord. 2010;29(1):37-45. doi: 10.1159/000257761. Epub 2010 Jan 27.
BACKGROUND/AIMS: The aim of this study was to map metabolic compensation and depression in Alzheimer's disease (AD) on a voxel-by-voxel basis.
Twenty-one healthy elderly subjects and 25 AD patients underwent cerebral MR and FDG-PET imaging. All images were processed with SPM2, and whole-brain gray matter (GM) atrophy and hypometabolism maps were computed. Metabolic compensation and depression were assessed using Biological Parametric Mapping software.
GM atrophy and hypometabolism mapped to similar regions, with varying degrees of severity. Significant metabolic compensation was found in the amygdala, while exceeding hypometabolism was mainly located in the posterior cingulate cortex.
Metabolic depression can be due to both distant effects of atrophy and to additional hypometabolism-inducing factors, such as amyloid deposition. Conversely, metabolic compensation could reflect spared synaptic plasticity of the surviving neurons. The investigation of the metabolic compensation mechanism could help in the comprehension of the AD underlying pathology.
背景/目的:本研究旨在对阿尔茨海默病(AD)进行基于体素的代谢代偿和抑郁分析。
21 名健康老年人和 25 名 AD 患者接受了脑部 MRI 和 FDG-PET 成像。所有图像均通过 SPM2 进行处理,并计算了全脑灰质(GM)萎缩和低代谢图。使用生物参数映射软件评估代谢代偿和抑郁情况。
GM 萎缩和低代谢映射到相似的区域,严重程度不同。在杏仁核中发现了明显的代谢代偿,而超过低代谢的区域主要位于后扣带皮层。
代谢抑制可能是由于萎缩的远距离影响以及淀粉样蛋白沉积等其他诱导低代谢的因素所致。相反,代谢代偿可能反映了存活神经元的未受损的突触可塑性。对代谢代偿机制的研究有助于理解 AD 的潜在病理。