title: Initial clinical comparison of 18F-florbetapir and 18F-FDG PET in patients with Alzheimer disease and controls.
abstract: The purpose of this study was to determine how clinical interpretations of the (18)F-amyloid tracer florbetapir compares diagnostically with (18)F-FDG PET when evaluating patients with Alzheimer disease (AD) and controls.
  
  
  METHODS
  Nineteen patients with a clinical diagnosis of AD and 21 elderly controls were evaluated with both (18)F-florbetapir and (18)F-FDG PET scans. Scans were interpreted together by 2 expert readers masked to any case information and were assessed for tracer binding patterns consistent with AD. The criteria for interpreting the (18)F-florbetapir scan as positive for AD was the presence of binding in the cortical regions relative to the cerebellum. (18)F-FDG PET scans were interpreted as positive if they displayed the classic pattern of hypometabolism in the temporoparietal regions. Scans were interpreted as either positive or negative for AD. In addition, a relative scoring system was used to assess the degree of either hypometabolism or amyloid binding in specified regions. The metabolism and amyloid binding scores for each region were compared across subjects. An overall ratio was calculated on the basis of values in regions expected to be affected by AD and those not expected to be affected. The metabolic ratio and amyloid ratio were then correlated with the mini-mental status examination (MMSE) score.
  
  
  RESULTS
  The sensitivity and specificity, compared with the clinical diagnosis of AD or controls, for the (18)F-florbetapir scans were 95% and 95%, respectively, and for the (18)F-FDG scans 89% and 86%, respectively. When a comparison with MMSE scores was made, (18)F-FDG significantly correlated with MMSE when both controls and AD patients were included (r = 0.79, P < 0.0001) and in AD patients alone (r = 0.70, P = 0.001). The (18)F-florbetapir scores significantly correlated with MMSE scores only when both controls and AD patients were included (r = 0.62, P < 0.001) but not in the AD group alone (r = 0.12, P = 0.66).
  
  
  CONCLUSIONS
  Overall, both scans performed well in detecting AD in patients with known clinical AD. Both scans correlated well with cognitive status as determined by MMSE when the entire cohort of controls and AD patients was evaluated. However, only the (18)F-FDG scans correlated with cognitive status when AD patients were evaluated separately.
authors.affiliation: Thomas Jefferson University and Hospital, Philadelphia, Pennsylvania 19107, USA. Andrew.newberg@jefferson.edu
authors.forename: Andrew B
authors.initials: AB
authors.lastname: Newberg
authors.forename: Steven E
authors.initials: SE
authors.lastname: Arnold
authors.forename: Nancy
authors.initials: N
authors.lastname: Wintering
authors.forename: Barry W
authors.initials: BW
authors.lastname: Rovner
authors.forename: Abass
authors.initials: A
authors.lastname: Alavi
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000544:Alzheimer Disease / Q000000981:diagnostic imaging*; D000814:Aniline Compounds; D005026:Ethylene Glycols; D005260:Female; D005462:Fluorine Radioisotopes; D019788:Fluorodeoxyglucose F18; D006801:Humans; D008297:Male; D008875:Middle Aged; D049268:Positron-Emission Tomography / Q000379:methods*; D019275:Radiopharmaceuticals; D012680:Sensitivity and Specificity; D012720:Severity of Illness Index
chemical_list: D000814:Aniline Compounds; D005026:Ethylene Glycols; D005462:Fluorine Radioisotopes; D019275:Radiopharmaceuticals; D019788:Fluorodeoxyglucose F18; C545186:florbetapir