ORCID Profile
0000-0002-8236-6561
Current Organisation
University of Sydney
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Publisher: Springer Science and Business Media LLC
Date: 13-09-2013
DOI: 10.1007/S11910-013-0396-6
Abstract: Logopenic progressive aphasia is the most recently described clinical variant of primary progressive aphasia (PPA), defined by impairment of lexical retrieval and sentence repetition. Unlike other PPA variants, the logopenic variant of PPA (lv-PPA) is commonly associated with Alzheimer's disease (AD), a fact that is relevant to the selection of patients for clinical trials and disease-modifying therapies. Despite the straightforward definition and coherent pathological association, the existence of lv-PPA has been challenged, as its distinction from AD or other PPA variants can be difficult. Despite these issues, lv-PPA patients display characteristic linguistic deficits, a pattern of brain atrophy, and possibly genetic susceptibility, which warrant considering this variant as a discrete AD endophenotype. More specific clinical and anatomical markers can strengthen the consistency of this syndrome.
Publisher: Elsevier BV
Date: 05-2017
DOI: 10.1016/J.NEUROIMAGE.2016.03.032
Abstract: Clinical differentiation between Alzheimer's disease (AD) and behavioural-variant frontotemporal dementia (bvFTD) is challenging due to overlapping clinical features at presentation. Whilst diagnostic criteria for both disorders incorporate evidence of frontal and temporal cortical atrophy, understanding of the progression of atrophy in these disorders is limited. This study aimed to elucidate common and disease-specific progressive changes in cortical and subcortical brain structures in AD and bvFTD. Forty-one AD, 37 bvFTD and 33 healthy controls underwent baseline MRI and of these longitudinal follow-up was obtained for 20AD and 20 bvFTD (1 to 4years). A total of 87 AD and 70 bvFTD consecutive scans were included in the study. The trajectories of progression in cortical and subcortical structures were identified with FreeSurfer and linear mixed effect modelling. The results uncovered cortical and subcortical disease-specific trajectories of neurodegeneration in AD and bvFTD. Specifically, direct comparisons between patient groups revealed that over time AD showed greater cortical atrophy in the inferior parietal and posterior cingulate cortex than bvFTD. Conversely, bvFTD patients showed greater atrophy in the striatum than AD over time. These results indicate that atrophy in the posterior cingulate and the striatum erges with disease progression in these dementia syndromes and may represent a potential diagnostic biomarker for tracking rates of progression of AD and bvFTD. These findings may help inform future drug trials by identifying appropriate outcome measures to quantify drug efficacy and their ability to modulate disease progression over time.
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 06-02-2013
Publisher: Negah Scientific Publisher
Date: 2018
Publisher: American Speech Language Hearing Association
Date: 10-2012
DOI: 10.1044/1092-4388(2012/11-0323)
Abstract: The International Consensus Criteria for the diagnosis of primary progressive aphasia (PPA Gorno-Tempini et al., 2011) propose apraxia of speech (AOS) as 1 of 2 core features of nonfluent/agrammatic PPA and propose phonological errors or absence of motor speech disorder as features of logopenic PPA. We investigated the sensitivity and specificity of AOS and phonological errors as markers for these variants and also investigated the relationship between AOS, phonological errors, and findings on C-labeled Pittsburgh Compound B (PiB)–positron emission tomography (PET) imaging associated with putative Alzheimer-type pathology. Connected speech and word repetition in 23 people with PPA who underwent PiB-PET imaging were rated for apraxic versus phonological disruption by 1 rater who was blind to diagnosis and by 2 raters who were blind to PiB-PET results. Apraxic characteristics had high sensitivity for nonfluent/agrammatic PPA, and phonological errors had high sensitivity for logopenic PPA however, phonological errors showed lower specificity for logopenic PPA. On PiB imaging, 8 of 9 people with predominant AOS returned negative results, whereas participants with no or questionable AOS with and without phonological errors returned positive results. Attention to AOS and phonological errors may help counter some of the inherent limitations of diagnosis-by-exclusion in the current International Consensus Criteria for diagnosing PPA.
Publisher: S. Karger AG
Date: 2012
DOI: 10.1159/000342347
Abstract: The longitudinal course of three primary progressive aphasia (PPA) variants was examined using Addenbrooke's Cognitive Examination-Revised (ACE-R) and the Frontotemporal dementia Rating Scale (FRS). Cases with two assessments on the ACE-R and FRS were selected. A total of 220 assessments were obtained on 55 patients: 17 Alzheimer's disease (AD) and 38 PPA [17 semantic variant (svPPA), 12 non-fluent/agrammatic (naPPA) and 9 logopenic variant (lvPPA) cases]. The annualized rate of change was greater in all PPA variants in comparison with the AD group on the ACE-R whereas only the svPPA and naPPA groups differed from AD on the FRS. The longitudinal profile differs across PPA syndromes on cognitive and functional measures. Findings have theoretical implications and are relevant to the care of patients with dementia.
Publisher: Oxford University Press (OUP)
Date: 09-09-2011
DOI: 10.1093/BRAIN/AWR216
Abstract: Primary progressive aphasia comprises a heterogeneous group of neurodegenerative conditions with erse clinical profiles and underlying pathological substrates. A major development has been the publication of the recent International Consensus Criteria for the three major variants namely: semantic, non-fluent/agrammatic and logopenic. The logopenic variant is assumed to represent an atypical presentation of Alzheimer pathology although evidence for this is, at present, limited. The semantic and non-fluent/agrammatic variants are largely associated with frontotemporal lobar degeneration with TDP-43 and tau pathology, respectively. The applicability of the International Consensus Criteria to an unselected clinical s le is unknown and no agreed clinical evaluation scale on which to derive the diagnosis exists. We assessed 47 consecutive cases of primary progressive aphasic seen over a 3-year period in a specialist centre, using a newly developed progressive aphasia language scale. A subgroup of 30 cases underwent (11)C-labelled Pittsburgh Compound B positron emission tomography imaging, a putative biomarker of Alzheimer's disease that detects β-amyloid accumulation, and they were compared with an age-matched group (n = 10) with typical, predominately amnestic Alzheimer's disease. The application of an algorithm based on four key speech and language variables (motor speech disorders, agrammatism, single-word comprehension and sentence repetition) classified 45 of 47 (96%) of patients and showed high concordance with the gold standard expert clinical diagnosis based on the International Consensus Criteria. The level of neocortical β-amyloid burden varied considerably across aphasic variants. Of 13 logopenic patients, 12 (92%) had positive β-amyloid uptake. In contrast, one of nine (11%) semantic variant and two of eight (25%) non-fluent/agrammatic cases were positive. The distribution of β-amyloid across cortical regions of interest was identical in cases with the logopenic variant to that of patients with typical Alzheimer's disease although the total load was lower in the aphasic cases. Impairments of sentence repetition and sentence comprehension were positively correlated with neocortical burden of β-amyloid, whereas impaired single-word comprehension showed a negative correlation. The International Consensus Criteria can be applied to the majority of cases with primary progressive aphasic using a simple speech and language assessment scale based upon four key variables. β-amyloid imaging confirms the higher rate of Alzheimer pathology in the logopenic variant and, in turn, the low rates in the other two variants. The study offers insight into the biological basis of clinical manifestations of Alzheimer's disease, which appear topographically independent of β-amyloid load.
Publisher: Society of Nuclear Medicine
Date: 06-08-2015
DOI: 10.2967/JNUMED.115.161067
Abstract: Alzheimer disease is the cause of up to one-third of cases of primary progressive aphasia or corticobasal syndrome. The primary objective of this study was to determine the accuracy of 18F-FDG PET metabolic imaging for the detection of Alzheimer disease in patients with primary progressive aphasia or corticobasal syndrome. A cohort of patients (n=94), including those with an expert clinical diagnosis of logopenic (n=19), nonfluent (n=16), or semantic (n=13) variants of primary progressive aphasia, corticobasal syndrome (n=14), or Alzheimer disease (n=24), underwent 18F-FDG metabolic and 11C-labeled Pittsburgh compound B (11C-PiB) amyloid PET brain imaging. 18F-FDG PET scans interpreted with Neurostat and 3D-SSP displays were classified as revealing Alzheimer disease or "other" by interpreters who were unaware of the clinical assessments and 11C-PiB PET results. 11C-PiB PET imaging was considered to be the diagnostic reference standard, with a threshold standardized uptake value ratio of 1.5 being indicative of Alzheimer disease pathology. To address possible bias from subgroup selection for the Alzheimer disease binary classifier, we calculated both conventional and balanced accuracies. Diagnoses of Alzheimer disease based on 18F-FDG PET resulted in 84% accuracy (both conventional and balanced). In comparison, diagnoses based on clinical assessments resulted in 65% conventional accuracy and 67% balanced accuracy. Brain 18F-FDG PET scans interpreted with Neurostat and 3D-SSP displays accurately detected Alzheimer disease in patients with primary progressive aphasia or corticobasal syndrome as focal-onset dementias. In such diagnostically challenging cohorts, (18)F-FDG PET imaging can provide more accurate diagnoses, enabling more appropriate therapy.
Publisher: Springer Science and Business Media LLC
Date: 04-03-2020
DOI: 10.1186/S13195-020-00587-5
Abstract: The Centiloid scale was developed to standardise the results of beta-amyloid (Aβ) PET. We aimed to determine the Centiloid unit (CL) thresholds for CERAD sparse and moderate-density neuritic plaques, Alzheimer’s disease neuropathologic change (ADNC) score of intermediate or high probability of Alzheimer’s Disease (AD), final clinicopathological diagnosis of AD, and expert visual read of a positive Aβ PET scan. Aβ PET results in CL for 49 subjects were compared with post-mortem findings, visual read, and final clinicopathological diagnosis. The Youden Index was used to determine the optimal CL thresholds from receiver operator characteristic (ROC) curves. A threshold of 20.1 CL (21.3 CL when corrected for time to death, AUC 0.97) yielded highest accuracy in detecting moderate or frequent plaque density while 10 CL was optimal for excluding neuritic plaque. The threshold for ADNC intermediate or high likelihood AD was 49.4 CL (AUC 0.98). Those cases with a final clinicopathological diagnosis of AD yielded a median CL result of 87.7 (IQR ± 42.2) with 94% 45 CL. Positive visual read agreed highly with results 26 CL. Centiloid values 10 accurately reflected the absence of any neuritic plaque and 20 CL indicated the presence of at least moderate plaque density, but approximately 50 CL or more best confirmed both neuropathological and clinicopathological diagnosis of Alzheimer’s disease.
Publisher: Oxford University Press (OUP)
Date: 12-09-2014
DOI: 10.1093/BRAIN/AWU246
Abstract: Disturbed emotion processing and difficulty with social interactions are present to variable degrees in dementia. They are characteristic features of frontotemporal dementia, whereas these deficits tend to be mild in Alzheimer's disease, reflecting the different patterns of neurodegeneration seen in these disorders. Corticobasal syndrome is an atypical parkinsonian disorder clinically and pathologically related to frontotemporal dementia. Corticobasal syndrome typically presents as a motor disturbance, although cognitive and behavioural changes are now recognized. Pathological changes are found in frontoparietal cortical regions and in the basal ganglia regions that are heavily involved in emotion processing. Despite the overlap with frontotemporal dementia and the observed regions of brain atrophy, emotion processing has not been systematically explored in corticobasal syndrome. This study aimed to (i) comprehensively examine emotion processing in corticobasal syndrome in comparison to Alzheimer's disease, to determine whether emotion processing deficits exist in this syndrome, beyond those seen in Alzheimer's disease and (ii) identify the neural correlates underlying emotion processing in corticobasal syndrome and Alzheimer's disease. Sixteen patients with corticobasal syndrome, 18 patients with Alzheimer's disease and 22 matched healthy control subjects were assessed on a comprehensive battery of face and emotion processing tasks. Behavioural analyses revealed deficits in both basic face processing and high-level emotion processing tasks in patients with corticobasal syndrome. Notably, the emotion processing disturbance persisted even after controlling for face processing deficits. In contrast, patients with Alzheimer's disease were impaired on high-level complex and cognitively demanding emotion recognition tasks (Ekman 60, The Awareness of Social Inference Test) only. Neuroimaging analyses using FreeSurfer revealed that emotion processing deficits in corticobasal syndrome were associated with basal ganglia volume loss as well as cortical thinning of the left paracentral gyrus recuneus region. In Alzheimer's disease, however, emotion processing deficits were associated with atrophy in a different set of brain regions, including the right cingulate and the bilateral insulae, as well as the hippoc i, right amygdala and nucleus accumbens bilaterally. Our results demonstrate that patients with corticobasal syndrome experience widespread deficits in emotion processing, and these deficits are related to changes in brain regions known to be crucial for emotion processing. These findings have important clinical implications for the treatment and management of these patients.
Publisher: S. Karger AG
Date: 2010
DOI: 10.1159/000313980
Abstract: i Background/Aims: /i Primary progressive aphasia (PPA) comprises 2 main variants: semantic dementia (SD) and progressive nonfluent aphasia (PNFA). Addenbrooke’s Cognitive Examination (ACE) has become widely used for the diagnosis of dementias. Less information, however, is available about its ability to detect and monitor changes in cognition in PPA. We aimed to analyse the sensitivity and longitudinal changes of ACE scores in 2 subforms of PPA. i Methods: /i We included 63 SD and 45 PNFA cases, all of whom had at least 2 assessments. Sensitivity levels, annualised rates of change and difference in scores over time on repeated ACE measurements were calculated. i Results: /i A cut-off of 88 points detected 95% of the PNFA and SD cases. Longitudinal analysis showed an average annual decline of 10 points per year, with no significant difference between groups. i Conclusion: /i The ACE is a useful tool for detecting and tracking the evolution of PPA.
Publisher: Elsevier BV
Date: 10-2016
DOI: 10.1016/J.CORTEX.2016.07.003
Abstract: Logopenic progressive aphasia (lv-PPA) is a form of primary progressive aphasia and is predominantly associated with Alzheimer's disease (AD) pathology. The neuropsychological profiles of lv-PPA and typical clinical AD are, however, distinct. In particular, these two syndromes differ on attention span measures, where auditory attention span is more impaired in lv-PPA than in AD and visuospatial span appears more impaired in AD than in lv-PPA. The neural basis of these span profiles, however, remains unclear. Sixteen lv-PPA and 21 AD matched patients, and 15 education-matched healthy controls were recruited. All participants were assessed by a neurologist and completed a neuropsychological assessment that included the Wechsler Memory Scale-III Digit and Spatial Span tasks, and underwent a high-resolution structural brain MRI to conduct cortical thickness analyses. Patient groups were impaired on all span tasks compared to Controls. In addition, performance on Digit Span Forward (DSF) was significantly lower in the lv-PPA than the AD group, while Spatial Span Forward (SSF) was significantly lower in the AD than the lv-PPA group. No differences were found between patient groups on the Digit or Spatial Span Backward tasks. Neuroimaging analyses revealed that reduced DSF performance correlated to thinning of the left superior temporal gyrus in the lv-PPA group, whereas reduced SSF performance was related to bilateral precentral sulcus and parieto-occipital thinning in the AD group. Analyses of the backward span tasks revealed that reduced Spatial Span Backward (SSB) performance in the lv-PPA group related to cortical thinning of the left superior parietal lobule. This study demonstrates that while lv-PPA and AD commonly share the same underlying neuropathology, their span profiles are distinct and are mediated by ergent patterns of cortical degeneration.
Publisher: Elsevier BV
Date: 2016
DOI: 10.1016/J.BPSC.2015.09.004
Abstract: Despite ergent clinical features, language and amnestic presentations of Alzheimer's disease (AD) appear to show comparable regional amyloid-β (Aβ) burden. By using a statistical network approach, we aimed to identify complex network patterns of Aβ deposition and explore the effect of apolipoprotein E (APOE) ε4 allele on cortical Aβ burden across AD phenotypes. Sixteen amnestic AD participants and 18 cases with logopenic-variant of primary progressive aphasia (lv-PPA) with a high cortical Aβ burden were selected. A comprehensive clinical assessment, Aβ imaging, and APOE genotyping were performed in all cases. Statistical network analysis was undertaken based on the estimation of sparse partial correlations of Aβ burden between cortical regions. Global and regional network statistical parameters as well as the effect of APOEε4 genotype on cortical Aβ were explored. The two groups showed equivalent distribution of cortical amyloid burden and frequency of APOEε4 genotype. Statistical network analysis, however, demonstrated ergent connectivity properties. The lv-PPA group demonstrated higher mean network degree and shorter characteristic path length than the amnestic AD group. Amnestic AD cases showed connectivity hubs confined to the mesial temporal and prefrontal lobes bilaterally, whereas lv-PPA cases showed hubs scattered across the whole cortical mantle. An interaction effect on total Aβ burden between APOE genotype and AD presentations was also detected. The network analysis reveals interregional network differences not evident using a simple comparison of Aβ burden. This suggests that regional neurotoxic effects may explain the phenotypical differences in AD presentation and that these can be modulated by APOE genotype.
Publisher: Oxford University Press (OUP)
Date: 04-07-2022
DOI: 10.1093/BRAINCOMMS/FCAC161
Abstract: The Addenbrooke’s Cognitive Examination III is a brief cognitive screening tool that is widely used for the detection and monitoring of dementia. Recent findings suggest that the three variants of primary progressive aphasia can be distinguished based on their distinct profiles on the five subdomain scores of this test. Here, we investigated the utility of the Addenbrooke’s Cognitive Examination III to differentiate the primary progressive aphasia variants based on their item-by-item performance profiles on this test. From these results, we created an interactive primary progressive aphasia Addenbrooke’s Cognitive Examination III calculator which predicts the variant based on a patient’s unique item-by-item profile. Twenty-eight logopenic variant, 25 non-fluent variant and 37 semantic variant primary progressive aphasia patients and 104 healthy controls completed the Addenbrooke’s Cognitive Examination III at first clinical presentation. Multinomial regression analyses were conducted to establish performance profiles among groups, and R Shiny from RStudio was used to create the interactive Addenbrooke’s Cognitive Examination III diagnostic calculator. To verify its accuracy, probability values of the regression model were derived based on a 5-fold cross-validation of cases. The calculator’s accuracy was then verified in an independent s le of 17 logopenic, 19 non-fluent and 13 semantic variant primary progressive aphasia patients and 68 Alzheimer’s disease patients who had completed the Addenbrooke’s Cognitive Examination III (or an older version of this test: Revised) and had in vivo amyloid-PET imaging and/or brain autopsy pathological confirmation. Cross-validation of cases in the calculator model revealed different rates of sensitivity in classifying variants: semantic = 100%, non-fluent = 80.6% and logopenic = 79.9% healthy controls were distinguished from primary progressive aphasia patients with 100% sensitivity. Verification of in vivo amyloid and/or autopsy-confirmed patients showed that the calculator correctly classified 10/13 (77%) semantic variant, 3/19 (16%) non-fluent variant and 4/17 (24%) logopenic variant patients. Importantly, for patients who were not classified, diagnostic probability values mostly pointed toward the correct clinical diagnosis. Furthermore, misclassified diagnoses of the primary progressive aphasia cohort were rare (1/49 2%). Although 22 of the 68 Alzheimer’s disease patients (32%) were misclassified with primary progressive aphasia, 19/22 were misclassified with the logopenic variant (i.e. falling within the same neuropathological entity). The Addenbrooke’s Cognitive Examination III primary progressive aphasia diagnostic calculator demonstrates sound accuracy in differentiating the variants based on an item-by-item Addenbrooke’s Cognitive Examination III profile. This calculator represents a new frontier in using data-driven approaches to differentiate the primary progressive aphasia variants.
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 19-07-2017
Publisher: S. Karger AG
Date: 2017
DOI: 10.1159/000478852
Abstract: b i Background/Aims: /i /b Although some patients with primary progressive aphasia (PPA) exhibit novel or improved skills after the onset of dementia, these changes have yet to be quantified. Therefore, this study systematically explored and identified the emergence of positive behaviours after dementia onset. b i Methods: /i /b This study included 48 carers of patients with PPA: 12 nonfluent/agrammatic PPA (nfvPPA), 22 semantic variant PPA (svPPA), and 14 logopenic variant PPA (lvPPA). The presence and frequency of positive behaviour changes after dementia onset were established using the Hypersensory and Social/Emotional Scale (HSS). b i Results: /i /b Scores on Sensitivity to Details, Visuospatial Activities, and Music Activities differed significantly among the groups. More specifically, svPPA was associated with increased visuospatial activity, but only in the mild stage of the disease nfvPPA was associated with increased visuospatial activity and decreased music activity, while lvPPA exhibited the reverse profile. b i Conclusions: /i /b The results demonstrate that subsets of PPA patients show novel or increased positive behaviours following dementia onset, and differences among subtypes may be helpful for improving diagnostic accuracy. Additionally, harnessing these skills may improve the quality of life of both patients and carers.
Publisher: Medknow
Date: 2010
Publisher: Informa UK Limited
Date: 03-01-2014
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 31-10-2018
Publisher: Elsevier BV
Date: 02-2016
DOI: 10.1016/J.NEUROBIOLAGING.2015.10.017
Abstract: Primary progressive aphasia (PPA) comprises a heterogeneous group of neurodegenerative conditions that can be classified in three cliniconeuroanatomic syndromes. Limited information exists, however, about patterns of neuropathologic spreading and microscopic changes underpinning each syndrome. We performed an analysis of a longitudinal in vivo cohort and a postmortem PPA cohort to investigate neurodegeneration over time and to quantify microscopic changes in key language brain areas. The longitudinal analyses demonstrated distinctive patterns of topological extension of brain atrophy. Although semantic variant (sv-PPA) showed an eccentric pattern, nonfluent and/or agrammatic (nfv-PPA) and logopenic (lv-PPA) variants showed additional multifocal extension. The quantitative pathology showed that sv-PPA had neuronal loss and thinning in BA 38, whereas nfv-PPA showed thinning in BA 44/45 and evidence of microscopic involvement in BA 40/22. Although lv-PPA showed neuronal loss focused on BA 40/22, imaging results demonstrated widespread left-sided brain atrophy. These analyses provide an account of the pathologic process whereby each variant has stereotypical patterns of brain atrophy extension, which is largely determined by the specific pathologic type.
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 17-04-2017
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 04-04-2014
Publisher: Elsevier BV
Date: 2017
DOI: 10.1016/J.CORTEX.2016.10.019
Abstract: The majority of logopenic variant primary progressive aphasia (lv-PPA) cases harbour Alzheimer pathology, suggesting that lv-PPA constitutes an atypical presentation of Alzheimer's disease (AD). However, even if caused by Alzheimer pathology, the clinical manifestations of lv-PPA differ from those observed in the typical or amnestic AD presentation: in lv-PPA, aphasia is the main feature while amnestic AD is characterised by impaired episodic memory. Anomia or impaired naming, however, is present in both AD presentations. Whether these presentations share anatomical and mechanistic processes of anomia has not been fully investigated. Accordingly, we studied naming performance and its relationship with regions of brain atrophy in 23 amnestic AD and 22 lv-PPA cases with presumed underlying Alzheimer pathology. Both AD groups displayed some degree of anomia and impaired word comprehension but these were particularly severe in lv-PPA and accompanied by a range of linguistic deficits, comprising phonological substitutions, superordinate semantic paraphasias and abnormal single-word repetition. Analysis of cortical thickness revealed that anomia was correlated with thinning in left superior temporal gyrus in both groups. In amnestic AD, however, anomia was also associated with thinning in right inferior temporal regions. Single-word comprehension (SWC), by contrast, was associated with cortical thinning involving bilateral fusiform gyri in both groups. These findings suggest that anomia in both amnestic AD and lv-PPA results from the involvement at multiple steps of word processing, in particular, semantic and lexical retrieval in addition lv-PPA patients display a more marked involvement of phonological processing.
Publisher: Public Library of Science (PLoS)
Date: 28-02-2014
Publisher: Informa UK Limited
Date: 23-11-2022
Publisher: Elsevier BV
Date: 06-2015
DOI: 10.1016/J.CORTEX.2015.03.011
Abstract: Logopenic progressive aphasia is one of the clinical presentations of primary progressive aphasia and formally defined by the co-occurrence of impaired naming and sentence repetition. Impaired naming is attributed to failure of lexical retrieval, which is a multi-staged process subserved by anatomically segregated brain regions. By dissecting the neurocognitive processes involved in impaired naming, we aimed to disentangle the clinical and neuroanatomical heterogeneity of this syndrome. Twenty-one in iduals (66.7% females, age range 53-83 years) who fulfilled diagnostic criteria for logopenic variant and had at least two clinical and language assessments, 1 year apart, were recruited and matched for age, sex distribution and level of education with a healthy control s le (n = 18). All participants underwent a structural brain scan at the first visit and surface-wise statistical analysis using Freesurfer. Seventeen participants with logopenic variant underwent amyloid imaging, with 14 demonstrating high amyloid retention. Based on their performance on single-word comprehension, repetition and confrontation naming, three subgroups of logopenic cases with distinctive linguistic profiles and distribution of atrophy were identified. The first subgroup (n = 10) demonstrated pure anomia and left-sided atrophy in the posterior inferior parietal lobule and lateral temporal cortex. The second subgroup (n = 6), presented additional mild deficits in single-word comprehension, and also exhibited bilateral thinning of the fusiform gyri. The third subgroup (n = 5) showed additional impaired single-word repetition, and cortical thinning focused on the left superior temporal gyrus. The subgroups differed in the proportion of cases with high amyloid retention and in the rate of decline of naming performance over time, suggesting that neurodegeneration spreads differentially throughout regions subserving word processing. In line with previous reports, these results confirm the extensive damage to the language network and, in part, explain the clinical heterogeneity observed across logopenic cases.
Publisher: Wiley
Date: 11-2018
DOI: 10.1002/ANA.25333
Start Date: 2016
End Date: 2020
Funder: National Health and Medical Research Council
View Funded ActivityStart Date: 2014
End Date: 2016
Funder: University of Sydney
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