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Article type: Research Article
Authors: Chamard, Ludivinea | Wallon, Davidb | Pijoff, Alexaa | Berger, Erica | Viennet, Gabrielc | Hannequin, Didierb | Magnin, Eloia; *
Affiliations: [a] Department of Neurology, Memory Resources and Research Center (CMRR), Besançon University Hospital, Besancon, France | [b] Department of Neurology, CNR-MAJ, INSERM 1079, Rouen University Hospital, Rouen, France | [c] Department of Anatomopathology, Besançon University Hospital, Besancon, France
Correspondence: [*] Correspondence to: Dr. Eloi Magnin, Department of Neurology, Memory Resources and Research Center, Besançon University Hospital, 25000 Besancon, France. Tel.: +33381668098; E-mail: eloi.magnin@laposte.net.
Abstract: Immune response to vascular amyloid-β deposits leads to cerebral amyloid angiopathy related-inflammation (CAA-ri). Amyloid-related imaging abnormalities (ARIA) were initially reported during anti-amyloid trials and are associated with the APOE 4/4 genotype. We report the evolution of an AβPP duplication carrier with an APOE 3/3 genotype presenting ARIA-Effusion and then ARIA-Hemosiderin deposit, without anti-amyloid therapy, suggestive of a possible spontaneously resolutive CAA-ri (not neuropathologically proven). It suggests common mechanisms between ARIA and CAA-ri and raises questions about mechanisms of this acute episode without APOE risk factor. The high vascular amyloid burden, induced by AβPP duplication, might increase amyloid epitope presentation and lead to inflammatory process.
Keywords: AβPP duplication, Alzheimer's disease, amyloid burden, APOE, cerebral amyloid angiopathy-related inflammation
DOI: 10.3233/JAD-130629
Journal: Journal of Alzheimer's Disease, vol. 37, no. 4, pp. 789-793, 2013
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