Document Detail


Distinct clinical and metabolic deficits in PCA and AD are not related to amyloid distribution.
MedLine Citation:
PMID:  21525424     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND/OBJECTIVE: Patients with posterior cortical atrophy (PCA) often have Alzheimer disease (AD) at autopsy, yet are cognitively and anatomically distinct from patients with clinical AD. We sought to compare the distribution of β-amyloid and glucose metabolism in PCA and AD in vivo using Pittsburgh compound B (PiB) and FDG-PET.
METHODS: Patients with PCA (n = 12, age 57.5 ± 7.4, Mini-Mental State Examination [MMSE] 22.2 ± 5.1), AD (n = 14, age 58.8 ± 9.6, MMSE 23.8 ± 6.7), and cognitively normal controls (NC, n = 30, age 73.6 ± 6.4) underwent PiB and FDG-PET. Group differences in PiB distribution volume ratios (DVR, cerebellar reference) and FDG uptake (pons-averaged) were assessed on a voxel-wise basis and by comparing binding in regions of interest (ROIs).
RESULTS: Compared to NC, both patients with AD and patients with PCA showed diffuse PiB uptake throughout frontal, temporoparietal, and occipital cortex (p < 0.0001). There were no regional differences in PiB binding between PCA and AD even after correcting for atrophy. FDG patterns in PCA and AD were distinct: while both groups showed hypometabolism compared to NC in temporoparietal cortex and precuneus/posterior cingulate, patients with PCA further showed hypometabolism in inferior occipitotemporal cortex compared to both NC and patients with AD (p < 0.05). Patients with AD did not show areas of relative hypometabolism compared to PCA.
CONCLUSIONS: Fibrillar amyloid deposition in PCA is diffuse and similar to AD, while glucose hypometabolism extends more posteriorly into occipital cortex. Further studies are needed to determine the mechanisms of selective network degeneration in focal variants of AD.
Authors:
M H Rosenbloom; A Alkalay; N Agarwal; S L Baker; J P O'Neil; M Janabi; I V Yen; M Growdon; J Jang; C Madison; E C Mormino; H J Rosen; M L Gorno-Tempini; M W Weiner; B L Miller; W J Jagust; G D Rabinovici
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2011-04-27
Journal Detail:
Title:  Neurology     Volume:  76     ISSN:  1526-632X     ISO Abbreviation:  Neurology     Publication Date:  2011 May 
Date Detail:
Created Date:  2011-05-24     Completed Date:  2011-07-22     Revised Date:  2014-09-20    
Medline Journal Info:
Nlm Unique ID:  0401060     Medline TA:  Neurology     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1789-96     Citation Subset:  AIM; IM    
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MeSH Terms
Descriptor/Qualifier:
Aged
Alzheimer Disease / metabolism*,  pathology,  physiopathology*
Amyloid beta-Peptides / metabolism*
Amyloid beta-Protein Precursor / metabolism
Cerebral Cortex / anatomy & histology,  metabolism*,  pathology,  physiopathology*
Female
Fluorodeoxyglucose F18 / metabolism
Glucose / metabolism
Humans
Male
Middle Aged
Positron-Emission Tomography
Syndrome
Grant Support
ID/Acronym/Agency:
K23 AG031861/AG/NIA NIH HHS; K23-AG031861/AG/NIA NIH HHS; P01-AG1972403/AG/NIA NIH HHS; P50 AG023501/AG/NIA NIH HHS; R01 NS050915/NS/NINDS NIH HHS; R01-AG027859/AG/NIA NIH HHS
Chemical
Reg. No./Substance:
0/APP protein, human; 0/Amyloid beta-Peptides; 0/Amyloid beta-Protein Precursor; 0Z5B2CJX4D/Fluorodeoxyglucose F18; IY9XDZ35W2/Glucose
Comments/Corrections
Comment In:
Neurology. 2011 May 24;76(21):1778-9   [PMID:  21525423 ]

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