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Interrelationship of superficial siderosis and microbleeds in cerebral amyloid angiopathy

2014; Lippincott Williams & Wilkins; Volume: 83; Issue: 20 Linguagem: Inglês

10.1212/wnl.0000000000000984

1526-632X

Ashkan Shoamanesh, Sergi Martínez‐Ramírez, Jamary Oliveira‐Filho, Yaël D. Reijmer, Guido J. Falcone, Alison Ayres, Kristin Schwab, Joshua N. Goldstein, Jonathan Rosand, M. Edip Gurol, Anand Viswanathan, Steven M. Greenberg,

Kruppel-like factors research

We sought to explore the mechanisms leading to cerebral amyloid angiopathy (CAA)-related cortical superficial siderosis (cSS) by examining its neuroimaging and genetic association with cerebral microbleeds (CMBs).MRI scans of 84 subjects with probable or definite CAA participating in a longitudinal research study were graded for cSS presence and severity (focal, restricted to ≤ 3 sulci vs disseminated, ≥ 4 sulci), and CMB count. APOE ε variants were directly genotyped. We performed cross-sectional analysis comparing CMB counts and APOE ε2 and ε4 allele frequency between subjects with no, focal, or disseminated cSS.cSS was present in 48% (n = 40) of the population. APOE ε2 was overrepresented among participants with focal (odds ratio [OR] 7.0, 95% confidence interval [CI] 1.7-29.3, p = 0.008) and disseminated (OR 11.5, 95% CI 2.8-46.2, p = 0.001) cSS relative to individuals without cSS. CMB counts decreased with increasing severity of cSS (median: 41, 38, and 15 for no cSS, focal cSS, and disseminated cSS, respectively, p = 0.09). The highest CMB count tertile was associated with APOE ε4 (OR 3.0, 95% CI 1.4-6.6, p = 0.006) relative to the lowest tertile.Among individuals with advanced CAA, cSS tends to occur in individuals with relatively lower CMB counts and with a distinct pattern of APOE genotypes. These results suggest that CAA-related cSS and CMBs may arise from distinct vasculopathic mechanisms.