Neuroinflammation and β Amyloid Deposition in Alzheimer's Disease: In vivo Quantification with Molecular Imaging

被引:20
|
作者
Hommet, C. [1 ,2 ,3 ]
Mondon, K. [1 ,2 ,3 ]
Camus, V. [1 ,2 ,3 ]
Ribeiro, M. J. [2 ,4 ]
Beaufils, E. [1 ,2 ]
Arlicot, N. [2 ,3 ]
Corcia, P. [2 ,3 ]
Paccalin, M. [5 ]
Minier, F. [2 ,3 ]
Gosselin, T. [2 ,3 ]
Page, G. [5 ]
Guilloteau, D. [2 ,3 ]
Chalon, S. [2 ,3 ]
机构
[1] Tours Univ Hosp, Memory Clin CMRR, FR-37044 Tours 9, France
[2] Univ Tours, Tours, France
[3] Inserm U930, Tours, France
[4] CHRU Tours, Nucl Med Unit, Tours, France
[5] Univ Poitiers, EA 3808, Poitiers, France
关键词
Neuroinflammation; Translocator protein; Microglia; Alzheimer's disease; Amyloid plaques; Molecular imaging; F-18]DPA-714; MILD COGNITIVE IMPAIRMENT; PERIPHERAL BENZODIAZEPINE-RECEPTOR; POSITRON-EMISSION-TOMOGRAPHY; PROTEIN; 18; KDA; WHITE-MATTER HYPERINTENSITIES; FLORBETAPIR F 18; MICROGLIAL ACTIVATION; ASSOCIATION WORKGROUPS; DIAGNOSTIC GUIDELINES; NATIONAL INSTITUTE;
D O I
10.1159/000354363
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: Neuroinflammation plays a crucial role in the pathogenesis of Alzheimer's disease (AD). Its relationship with underlying beta amyloid deposition remains unclear. In vivo visualization of microglial activation has become possible with the development of molecular imaging ligands when used with positron emission tomography (PET). The translocator protein (TSPO) is upregulated during neuroinflammation. Consequently, targeting TSPO with radiolabeled ligands for PET is an attractive biomarker for neuroinflammation. Methods: A review of the research literature on PET imaging which studied in vivo neuroinflammation in AD subjects and its relationship with amyloid load was performed, including papers published between 2001 and 2012. Results: Six studies were included using either [C-11]PK-11195 or another non-TSPO radioligand that binds to the monoaminooxidase B. All the studies evaluated amyloid load with [C-11]PIB. Microglial activation and astrocytosis are potentially early phenomena in AD. However, the individual levels of amyloid deposition and microglial activation were not correlated. Conclusion: Noninvasive in vivo molecular imaging to visualize neuroinflammation in AD may contribute to our understanding of the kinetics of neuroinflammation and its relationship to the hallmarks of the disease. Both are important for the development of future therapeutic modalities and for quantifying the efficacy of future disease-modifying treatments. (C) 2013 S. Karger AG, Basel
引用
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页码:1 / 18
页数:18
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