Metabolic Compensation and Depression in Alzheimer's Disease

被引：16

作者：

Caroli, A. ^{[1
,6
]}

Lorenzi, M. ^{[1
]}

Geroldi, C. ^{[1
,2
]}

Nobili, F. ^{[7
]}

Paghera, B. ^{[4
]}

Bonetti, M. ^{[5
]}

Cotelli, M. ^{[3
]}

Frisoni, G. B. ^{[1
,2
,8
]}

机构：

[1] FBF, IRCCS S Giovanni di Dio, LENITEM Lab Epidemiol Neuroimaging & Telemed, IT-25125 Brescia, Italy

[2] FBF, IRCCS S Giovanni di Dio, Psychogeriatr Unit, IT-25125 Brescia, Italy

[3] FBF, IRCCS S Giovanni di Dio, Cognit Neurosci Sect, IT-25125 Brescia, Italy

[4] Spedali Civil Brescia, Dept Nucl Med, I-25125 Brescia, Italy

[5] Clin Inst Citta Brescia, Serv Neuroradiol, Brescia, Italy

[6] Mario Negri Inst Pharmacol Res, Dept Biomed Engn, Med Imaging Unit, I-24100 Bergamo, Italy

[7] Univ Genoa, Dept Endocrinol & Med Sci, Div Clin Neurophysiol, Genoa, Italy

[8] AFaR Assoc Fatebenefratelli Ric, Rome, Italy

来源：

DEMENTIA AND GERIATRIC COGNITIVE DISORDERS | 2010年 / 29卷 / 01期

关键词：

Alzheimer's disease; Positron emission tomography; Magnetic resonance imaging; Atrophy-hypometabolism mismatch; Voxel-based analysis; MILD COGNITIVE IMPAIRMENT; MATTER HYPOMETABOLISM; SYNAPTIC PLASTICITY; DIAGNOSTIC-VALUE; FDG-PET; BRAIN; ATROPHY; MRI;

D O I：

10.1159/000257761

中图分类号：

R592 [老年病学]; C [社会科学总论];

学科分类号：

03 ; 0303 ; 100203 ;

摘要：

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. Methods: Twenty-one heal thy 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. Results: 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. Conclusion: 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. Copyright (C) 2010 S. Karger AG, Basel

引用

页码：37 / 45

页数：9

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