title: Regional glucose metabolic reduction in dementia with Lewy bodies is independent of amyloid deposition.
abstract: OBJECTIVE
  There is evidence that some cases of patients with dementia with Lewy bodies (DLB) can demonstrate Alzheimer disease (AD) like reduced glucose metabolism without amyloid deposition. The aim of this study was to clarify whether regional hypometabolism is related to amyloid deposits in the DLB brain and measure the degree of regional hypometabolism.
  
  
  METHODS
  Ten consecutive subjects with DLB and 10 AD patients who underwent both Pittsburgh compound B (PiB)-PET and (18)F-fluoro-2-deoxyglucose (FDG)-PET were included in this study. Regional standardized uptake value ratio (SUVR)s normalised to cerebellar cortices were calculated in the FDG- and PiB-PET images.
  
  
  RESULTS
  All AD patients and five DLB patients showed amyloid deposits (PiB positive). In the DLB group the parietotemporal and occipital metabolism were significantly lower than those in the AD group but there was no difference between the posterior cingulate hypometabolism between DLB and AD groups. There were no differences in regional glucose metabolism between PiB positive and negative DLB patients.
  
  
  CONCLUSIONS
  In the DLB brain, it is suggested that decreased regional glucose metabolism is unrelated to amyloid deposits, although the hypometabolic area overlaps with the AD hypometabolic area and the degree of parietotemporal and occipital hypometabolism in DLB brain is much larger than that in AD brain.
authors.affiliation: Neurocognitive Disorders Center, Kinki University Hospital, 377-2 Ohnohigashi, Osakasayama, Osaka, 589-8511, Japan, ishii@med.kindai.ac.jp.
authors.forename: Kazunari
authors.initials: K
authors.lastname: Ishii
authors.forename: Chisa
authors.initials: C
authors.lastname: Hosokawa
authors.forename: Tomoko
authors.initials: T
authors.lastname: Hyodo
authors.forename: Kenta
authors.initials: K
authors.lastname: Sakaguchi
authors.forename: Kimio
authors.initials: K
authors.lastname: Usami
authors.forename: Kenji
authors.initials: K
authors.lastname: Shimamoto
authors.forename: Makoto
authors.initials: M
authors.lastname: Hosono
authors.forename: Yuzuru
authors.initials: Y
authors.lastname: Yamazoe
authors.forename: Takamichi
authors.initials: T
authors.lastname: Murakami
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000544:Alzheimer Disease / Q000000981:diagnostic imaging / Q000378:metabolism*; D000682:Amyloid / Q000378:metabolism*; D000814:Aniline Compounds; D052160:Benzothiazoles; D001921:Brain / Q000000981:diagnostic imaging / Q000378:metabolism*; D001931:Brain Mapping; D005260:Female; D019788:Fluorodeoxyglucose F18; D005947:Glucose / Q000378:metabolism*; D006801:Humans; D020961:Lewy Body Disease / Q000000981:diagnostic imaging / Q000378:metabolism*; D008297:Male; D011877:Radionuclide Imaging; D019275:Radiopharmaceuticals; D013844:Thiazoles
chemical_list: C475519:2-(4'-(methylamino)phenyl)-6-hydroxybenzothiazole; D000682:Amyloid; D000814:Aniline Compounds; D052160:Benzothiazoles; D019275:Radiopharmaceuticals; D013844:Thiazoles; D019788:Fluorodeoxyglucose F18; D005947:Glucose