title: Decreased hippocampal metabolism in high-amyloid mild cognitive impairment.
abstract: Hippocampal volume (HV), cortical metabolism, and thickness are decreased in mild cognitive impairment (MCI). Hippocampal metabolism (HM) studies comparing MCI and clinically normal (CN) elderly gave inconsistent results. As hippocampus is a key region in Alzheimer's disease, we hypothesized that HM is specifically decreased in high-amyloid MCI.
  
  
  
  Overall, 250 CN and 45 MCI underwent three-dimensional magnetic resonance imaging, fludeoxyglucose-positron emission tomography, and fluorodeoxyglucose-positron emission tomography (PET), and Pittsburgh Compound B (PiB) PET. We investigated the interaction between clinical and amyloid status on HM, HV, cortical metabolism, and thickness using linear models, covarying age, gender, and education. Analyses were conducted with and without correction for multiple comparisons and for partial volume effects.
  
  
  
  Volume-adjusted HM was decreased in high-amyloid MCI but close to normal in low-amyloid MCI and in high-amyloid CN. Both MCI groups had hippocampal atrophy, although less severe in low-amyloid MCI. High-amyloid CN and high-amyloid MCI had cortical hypometabolism.
  
  
  
  HM is decreased when both cognitive impairment and amyloid are present.
authors.affiliation: Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA; Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA; The Martinos Center for Biomedical Imaging, Charlestown, MA, USA. Electronic address: bhanseeuw@mgh.harvard.edu.
authors.forename: Bernard J
authors.initials: BJ
authors.lastname: Hanseeuw
authors.affiliation: Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA; Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA; The Martinos Center for Biomedical Imaging, Charlestown, MA, USA.
authors.forename: Aaron P
authors.initials: AP
authors.lastname: Schultz
authors.affiliation: Department of Biostatistics, Harvard T.H. Chan School of Public Health, Boston, MA, USA.
authors.forename: Rebecca A
authors.initials: RA
authors.lastname: Betensky
authors.affiliation: Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA; Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA; The Martinos Center for Biomedical Imaging, Charlestown, MA, USA.
authors.forename: Reisa A
authors.initials: RA
authors.lastname: Sperling
authors.affiliation: Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA; Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA; The Martinos Center for Biomedical Imaging, Charlestown, MA, USA.
authors.forename: Keith A
authors.initials: KA
authors.lastname: Johnson
mesh_terms: D000368:Aged; D000682:Amyloid / Q000378:metabolism*; D000814:Aniline Compounds; D001284:Atrophy / Q000473:pathology; D060825:Cognitive Dysfunction / Q000000981:diagnostic imaging* / Q000378:metabolism / Q000473:pathology*; D005260:Female; D019788:Fluorodeoxyglucose F18; D006624:Hippocampus / Q000378:metabolism* / Q000473:pathology; D006801:Humans; D007091:Image Processing, Computer-Assisted; D008297:Male; D049268:Positron-Emission Tomography; D013844:Thiazoles
chemical_list: C475519:2-(4'-(methylamino)phenyl)-6-hydroxybenzothiazole; D000682:Amyloid; D000814:Aniline Compounds; D013844:Thiazoles; D019788:Fluorodeoxyglucose F18
keywords: Alzheimer's disease; Amyloid; Association cortex; FDG-PET; Hippocampus; Metabolism; Mild cognitive impairment