title: MR imaging features of amyloid-related imaging abnormalities.
abstract: OBJECTIVE
  AD is one of the few leading causes of death without a disease-modifying drug; however, hopeful agents are in various phases of development. MR imaging abnormalities, collectively referred to as amyloid-related imaging abnormalities, have been reported for several agents that target cerebral Aβ burden. ARIA includes ARIA-E, parenchymal or sulcal hyperintensities on FLAIR indicative of parenchymal edema or sulcal effusions, and ARIA-H, hypointense regions on gradient recalled-echo/T2* indicative of hemosiderin deposition. This report describes imaging characteristics of ARIA-E and ARIA-H identified during studies of bapineuzumab, a humanized monoclonal antibody against Aβ.
  
  
  METHODS
  Two neuroradiologists with knowledge of imaging changes reflective of ARIA reviewed MR imaging scans from 210 bapineuzumab-treated patients derived from 3 phase 2 studies. Each central reader interpreted the studies independently, and discrepancies were resolved by consensus. The inter-reader κ was 0.76, with 94% agreement between neuroradiologists regarding the presence or absence of ARIA-E in individual patients.
  
  
  RESULTS
  Thirty-six patients were identified with incident ARIA-E (17.1%, 36/210) and 26 with incident ARIA-H (12.4%, 26/210); of those with incident ARIA-H, 24 had incident microhemorrhages and 2 had incident large superficial hemosiderin deposits.
  
  
  CONCLUSIONS
  In 49% of cases of ARIA-E, there was the associated appearance of ARIA-H. In treated patients without ARIA-E, the risk for incident blood products was 4%. This association between ARIA-E and ARIA-H may suggest a common pathophysiologic mechanism. Familiarity with ARIA should permit radiologists and clinicians to recognize and communicate ARIA findings more reliably for optimal patient management.
authors.affiliation: California Pacific Medical Center, San Francisco, California.
authors.forename: J
authors.initials: J
authors.lastname: Barakos
authors.forename: R
authors.initials: R
authors.lastname: Sperling
authors.forename: S
authors.initials: S
authors.lastname: Salloway
authors.forename: C
authors.initials: C
authors.lastname: Jack
authors.forename: A
authors.initials: A
authors.lastname: Gass
authors.forename: J B
authors.initials: JB
authors.lastname: Fiebach
authors.forename: D
authors.initials: D
authors.lastname: Tampieri
authors.forename: D
authors.initials: D
authors.lastname: Melançon
authors.forename: Y
authors.initials: Y
authors.lastname: Miaux
authors.forename: G
authors.initials: G
authors.lastname: Rippon
authors.forename: R
authors.initials: R
authors.lastname: Black
authors.forename: Y
authors.initials: Y
authors.lastname: Lu
authors.forename: H R
authors.initials: HR
authors.lastname: Brashear
authors.forename: H M
authors.initials: HM
authors.lastname: Arrighi
authors.forename: K A
authors.initials: KA
authors.lastname: Morris
authors.forename: M
authors.initials: M
authors.lastname: Grundman
mesh_terms: D000544:Alzheimer Disease / Q000188:drug therapy* / Q000453:epidemiology / Q000473:pathology*; D016229:Amyloid beta-Peptides / Q000378:metabolism; D000686:Amyloidosis / Q000139:chemically induced* / Q000453:epidemiology / Q000473:pathology*; D061067:Antibodies, Monoclonal, Humanized / Q000008:administration & dosage / Q000009:adverse effects*; D001921:Brain / Q000378:metabolism / Q000473:pathology; D001929:Brain Edema / Q000453:epidemiology / Q000473:pathology; D002543:Cerebral Hemorrhage / Q000453:epidemiology / Q000473:pathology; D017322:Clinical Trials, Phase II as Topic; D005682:Gadolinium; D006485:Hemosiderin / Q000378:metabolism; D006801:Humans; D015994:Incidence; D008279:Magnetic Resonance Imaging; D016032:Randomized Controlled Trials as Topic; D012307:Risk Factors; D012720:Severity of Illness Index
chemical_list: D016229:Amyloid beta-Peptides; D061067:Antibodies, Monoclonal, Humanized; D006485:Hemosiderin; D005682:Gadolinium; C545458:bapineuzumab