Cerebrospinal Fluid, MRI, and Florbetaben-PET in Cerebral Amyloid Angiopathy-Related Inflammation

被引:15
|
作者
Renard, Dimitri [1 ]
Collombier, Laurent [2 ]
Demattei, Christophe [3 ]
Wacongne, Anne [1 ]
Charif, Mahmoud [4 ]
Ayrignac, Xavier [4 ]
Azakri, Souhayla [4 ]
Gaillard, Nicolas [5 ]
Boudousq, Vincent [2 ]
Lehmann, Sylvain [6 ]
de Champfleur, Nicolas Menjot [7 ]
Thouvenot, Eric [1 ,8 ]
机构
[1] CHU Nimes, Hop Caremeau, Dept Neurol, 4 Rue Pr Debre, F-30029 Nimes 4, France
[2] CHU Nimes, Hop Caremeau, Dept Nucl Med, Nimes, France
[3] CHU Nimes, Hop Caremeau, Dept Biostat BESPIM, Nimes, France
[4] CHU Montpellier, Hop Gui Chauliac, Dept Neurol, Montpellier, France
[5] CH Perpignan, Dept Neurol, Perpignan, France
[6] Univ Montpellier, CHU Montpellier, Lab Biochim Proteomique Clin, Hop St Eloi,IRMB,CRB,Inserm,U11183, Montpellier, France
[7] CHU Nimes, Hop Caremeau, Dept Med Imaging, Nimes, France
[8] Univ Montpellier, UMR5203, Inst Genom Fonct, Montpellier, France
关键词
Amyloid; florbetaben; imaging; BETA-RELATED ANGIITIS; POSITRON-EMISSION-TOMOGRAPHY; CENTRAL-NERVOUS-SYSTEM; PITTSBURGH COMPOUND-B; ALZHEIMERS-DISEASE; SUPERFICIAL SIDEROSIS; COGNITIVE IMPAIRMENT; CSF BIOMARKER; QUANTIFICATION; MICROBLEEDS;
D O I
10.3233/JAD-170843
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Background: Cerebral amyloid angiopathy-related inflammation (CAA-ri) is associated with a cerebrospinal fluid (CSF) biomarker profile similar to that observed in CAA. Few CAA-ri patients have been studied by fibrillar amyloid-beta (A beta) imaging (using C-11-Pittsburgh compound B and F-18-florbetapir, but not F-18-florbetaben). Objective: To describe CSF biomarkers, magnetic resonance imaging (MRI), and F-18-florbetaben (FBB)-positron emission tomography (PET) changes in CAA-ri patients. Methods: CSF levels of total tau, phosphorylated tau, A beta(1-42), and A beta(1-40), MRI (cerebral microbleeds count on susceptibility-weighted imaging and semi-quantitative analysis of fluid-attenuation inversion recovery white matter hyperintensities), and FBB-PET (using both cerebellar cortex and pons to calculate standardized uptake value ratios) were analyzed in nine consecutive CAA-ri patients. Results: A median number of 769 cerebral microbleeds/patient were counted on MRI. When using the pons as reference region, amyloid load on FBB-PET was very strongly correlated to CSF A beta(1-40) levels (rho = -0.83, p = 0.008) and moderately correlated to cerebral microbleed numbers in the occipital lobes (rho = 0.59, p = 0.001), while comparisons with other CSF biomarkers were not statistically significant (total tau, rho = -0.63, p = 0.076; phosphorylated tau, rho = -0.68, p = 0.05; A beta(1-42), rho = -0.59, p = 0.09). All correlations were weaker, and not statistically significant, when using the cerebellum as reference region. A non-significant correlation (rho = -0.50, p = 0.18) was observed between CSF A beta(1-40) levels and cerebral microbleed numbers. Conclusion: In CAA-ri, CSF A beta(1-40) levels correlated well with amyloid load assessed by FBB-PET when the pons was used as reference, and to a lesser degree with cerebral microbleeds count on MRI. This confirms earlier data on CSF A beta(1-40) as an in vivo marker for CAA and CAA-ri.
引用
收藏
页码:1107 / 1117
页数:11
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