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. 2008 Oct;64(4):388-401.
doi: 10.1002/ana.21451.

Abeta amyloid and glucose metabolism in three variants of primary progressive aphasia

Gil D Rabinovici  1 , William J Jagust, Ansgar J Furst, Jennifer M Ogar, Caroline A Racine, Elizabeth C Mormino, James P O'Neil, Rayhan A Lal, Nina F Dronkers, Bruce L Miller, Maria Luisa Gorno-Tempini
Affiliations

Abeta amyloid and glucose metabolism in three variants of primary progressive aphasia

Gil D Rabinovici et al. Ann Neurol. 2008 Oct.

Abstract

Objective: Alzheimer's disease (AD) is found at autopsy in up to one third of patients with primary progressive aphasia (PPA), but clinical features that predict AD pathology in PPA are not well defined. We studied the relationships between language presentation, Abeta amyloidosis, and glucose metabolism in three PPA variants using [11C]-Pittsburgh compound B ([11C]PIB) and [18F]-labeled fluorodeoxyglucose positron emission tomography ([18F]FDG-PET).

Methods: Patients meeting PPA criteria (N = 15) were classified as logopenic aphasia (LPA), progressive nonfluent aphasia (PNFA), or semantic dementia (SD) based on language testing. [11C]PIB distribution volume ratios were calculated using Logan graphical analysis (cerebellar reference). [18F]FDG images were normalized to pons. Partial volume correction was applied.

Results: Elevated cortical PIB (by visual inspection) was more common in LPA (4/4 patients) than in PNFA (1/6) and SD (1/5) (p < 0.02). In PIB-positive PPA, PIB uptake was diffuse and indistinguishable from the pattern in matched AD patients (n = 10). FDG patterns were focal and varied by PPA subtype, with left temporoparietal hypometabolism in LPA, left frontal hypometabolism in PNFA, and left anterior temporal hypometabolism in SD. FDG uptake was significant asymmetric (favoring left hypometabolism) in PPA (p < 0.005) but not in AD.

Interpretation: LPA is associated with Abeta amyloidosis, suggesting that subclassification of PPA based on language features can help predict the likelihood of AD pathology. Language phenotype in PPA is closely related to metabolic changes that are focal and anatomically distinct between subtypes, but not to amyloid deposition patterns that are diffuse and similar to AD.

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Figures

Fig 1
Fig 1
Distribution of PIB in PPA. Axial slices (z = 9, z = 27, z = 41) of normalized, atrophy-corrected PIB DVR images from single PIB-positive (left column) and PIB-negative (right column) PPA patients are presented. Identical slices from mean atrophy-corrected PIB DVR images from patients with AD (N = 10, top left) and normal controls (N = 12, top right) are shown for comparison. Images are in neurological orientation.
Fig 2
Fig 2
Mean lateralization indices (LI) for (A) PIB and (B) FDG. Bar graphs represent mean ± standard error for each PPA subtype and for AD in frontal (Front), anterior temporal (AntTemp), temporoparietal (TempPar) and Cumulative PPA (Mean PPA) regions of interest. Asterisks mark values significantly different than 0 indicating lateralization (p<0.05, one sample two-tailed t-test).
Fig 3
Fig 3
FDG patterns by clinical syndrome. Axial (z = 9, z = 27) and coronal (y = 64) slices of mean atrophy-corrected FDG images from (top to bottom) normal controls (N = 12), PNFA (N = 5), SD (N = 5), LPA (N = 4) and AD (N = 10). Images are in neurological orientation. PNFA is characterized by left frontal hypometabolism (red arrow), SD by left greater than right anterior temporal hypometabolism (yellow arrows), and LPA by asymmetric left temporoparietal hypometabolism (light blue arrows).
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