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

Article type: Research Article

Authors: Renard, Dimitri^{a; *} | Collombier, Laurent^b | Demattei, Christophe^c | Wacongne, Anne^a | Charif, Mahmoud^d | Ayrignac, Xavier^d | Azakri, Souhayla^d | Gaillard, Nicolas^e | Boudousq, Vincent^b | Lehmann, Sylvain^f | Menjot de Champfleur, Nicolas^g | Thouvenot, Eric^{a; h}

Affiliations: [a] Department of Neurology, CHU Nîmes, Hôpital Caremeau, France | [b] Department of Nuclear Medicine, CHU Nîmes, Hôpital Caremeau, France | [c] Department of Biostatistics (BESPIM), CHU Nîmes, Hôpital Caremeau, France | [d] Department of Neurology, CHU Montpellier, Hôpital Gui de Chauliac, France | [e] Department of Neurology, CH Perpignan, France | [f] Laboratoire de Biochimie-Protéomique Clinique – IRMB – CRB – Inserm U11183, CHU Montpellier, Hôpital St-Eloi – Université Montpellier, France | [g] Department of Medical Imaging, CHU Nîmes, Hôpital Caremeau, France | [h] Institut de Génomique Fonctionnelle, UMR5203, Université Montpellier, Montpellier, France

Correspondence: [*] Correspondence to: Dimitri Renard, MD, Department of Neurology, CHU Nîmes, Hôpital Caremeau, 4, Rue du Pr Debré, 30029 Nîmes Cedex 4, France. Tel.: +33 4 66 68 32 61; Fax: +33 4 66 68 40 16; E-mail: dimitrirenard@hotmail.com.

Abstract: 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-β (Aβ) imaging (using 11C-Pittsburgh compound B and 18F-florbetapir, but not 18F-florbetaben). Objective:To describe CSF biomarkers, magnetic resonance imaging (MRI), and 18F-florbetaben (FBB)-positron emission tomography (PET) changes in CAA-ri patients. Methods:CSF levels of total tau, phosphorylated tau, Aβ1-42, and Aβ1-40, 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 Aβ1-40 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; Aβ1-42, 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 Aβ1-40 levels and cerebral microbleed numbers. Conclusion:In CAA-ri, CSF Aβ1-40 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 Aβ1-40 as an in vivo marker for CAA and CAA-ri.

Keywords: Amyloid, florbetaben, imaging

DOI: 10.3233/JAD-170843

Journal: Journal of Alzheimer's Disease, vol. 61, no. 3, pp. 1107-1117, 2018