Abstract
ObjectivesThe logopenic variant of primary progressive aphasia is an atypical clinical variant of Alzheimer’s disease which is typically characterized by left temporoparietal atrophy on magnetic resonance imaging and hypometabolism on F-18 fluorodeoxyglucose positron emission tomography. We aimed to characterize and compare patterns of atrophy and hypometabolism in logopenic primary progressive aphasia, and determine which brain regions and imaging modality best differentiates logopenic primary progressive aphasia from typical dementia of the Alzheimer’s type.MethodsA total of 27 logopenic primary progressive aphasia subjects underwent fluorodeoxyglucose positron emission tomography and volumetric magnetic resonance imaging. These subjects were matched to 27 controls and 27 subjects with dementia of the Alzheimer’s type. Patterns of atrophy and hypometabolism were assessed at the voxel and region-level using Statistical Parametric Mapping. Penalized logistic regression analysis was used to determine what combinations of regions best discriminate between groups.ResultsAtrophy and hypometabolism was observed in lateral temporoparietal and medial parietal lobes, left greater than right, and left frontal lobe in the logopenic group. The logopenic group showed greater left inferior, middle and superior lateral temporal atrophy (inferior p = 0.02; middle p = 0.007, superior p = 0.002) and hypometabolism (inferior p = 0.006, middle p = 0.002, superior p = 0.001), and less right medial temporal atrophy (p = 0.02) and hypometabolism (p<0.001), and right posterior cingulate hypometabolism (p<0.001) than dementia of the Alzheimer’s type. An age-adjusted penalized logistic model incorporating atrophy and hypometabolism achieved excellent discrimination (area under the receiver operator characteristic curve = 0.89) between logopenic and dementia of the Alzheimer’s type subjects, with optimal discrimination achieved using right medial temporal and posterior cingulate hypometabolism, left inferior, middle and superior temporal hypometabolism, and left superior temporal volume.ConclusionsPatterns of atrophy and hypometabolism both differ between logopenic primary progressive aphasia and dementia of the Alzheimer’s type and both modalities provide excellent discrimination between groups.
Highlights
Primary progressive aphasia (PPA) is a language disorder that is characterized by deficits in functions such as object naming, syntax, and word-processing [1]
We selected only subjects who had a positive Pittsburgh Compund B (PiB)-PET scan demonstrating the probable presence of Alzheimer’s disease (AD) pathology, since there is a suggestion that patterns of atrophy may differ between logopenic variant of PPA (lvPPA) subjects with and without AD pathology [13,14]
Median global PiB ratios were lower in controls than lvPPA and dementia of the Alzheimer’s type (DAT), but did not differ between lvPPA and DAT
Summary
Primary progressive aphasia (PPA) is a language disorder that is characterized by deficits in functions such as object naming, syntax, and word-processing [1]. In contrast to patients with the agrammatic and semantic variants, the majority of subjects with the logopenic variant of PPA (lvPPA) have been shown at autopsy or using amyloid-binding ligands such as Pittsburgh Compund B (PiB) [3] to have Alzheimer’s disease (AD) pathology [4,5,6]. Similar and overlapping patterns of temporoparietal atrophy have been observed in DAT [9,10]. Patterns of hypometabolism on F-18-fluorodeoxyglucose (FDG) PET have been reported in only a handful of lvPPA patients (n = 10), with similar patterns of left temporoparietal involvement observed [4,12]. Comparing the structural and functional abnormalities of these two syndromes would help increase understanding of the mechanisms that drive heterogeneity in AD, and would be important for future studies evaluating environmental or genetic risk and monitoring progression in these syndromes
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