Biomarkers for diseases with TDP-43 pathology

Steinacker, Petra; Barschke, Peggy; Otto, Markus

doi:10.1016/j.mcn.2018.10.003

Cited by 47 publications

(38 citation statements)

References 236 publications

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“…Optimal biomarkers for LATE, including biofluids or PET ligands, would be specific for the disease-defining feature, namely TDP-43 proteinopathy (Steinacker et al , 2018). At this time, no biofluid or PET biomarker satisfies this essential criterion of molecular specificity.…”

Section: Introductionmentioning

confidence: 99%

Limbic-predominant age-related TDP-43 encephalopathy (LATE): consensus working group report

Nelson

Dickson

Trojanowski

et al. 2019

Brain

980

1,035

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Nelson et al. describe a recently recognized brain disorder that mimics the clinical features of Alzheimer’s disease: L imbic-predominant A ge-related T DP-43 E ncephalopathy (LATE). They review the literature and present consensus-based recommendations of an international, multidisciplinary working group, providing guidelines for diagnosis and staging of LATE neuropathological changes.

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Section: Introductionmentioning

confidence: 99%

Limbic-predominant age-related TDP-43 encephalopathy (LATE): consensus working group report

Nelson

Dickson

Trojanowski

et al. 2019

Brain

980

1,035

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“…In the future, diagnostic help could come from [18F]AV-1451 PET (so called TAU PET) which seems to bind to bilateral temporal lobe pathology in svPPA cases, but does not show frontal/temporal binding in bvFTD ( Bevan-Jones et al, 2018 , Josephs et al, 2018 , Makaretz et al, 2018 ). However, to date no biomarker for TDP exists ( Steinacker et al, 2019 ), so the integration of clinical and neuroimaging findings is still the best way to diagnose these patients. Regarding therapy trials, the implications of our findings are two-folds.…”

Section: Discussionmentioning

confidence: 99%

Regional and hemispheric susceptibility of the temporal lobe to FTLD-TDP type C pathology

Borghesani

Battistella

Mandelli

et al. 2020

NeuroImage: Clinical

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Highlights Anterior temporal lobe (ATL) degeneration is most often caused by FTLD-TDP type C pathology. Cases can present with predominantly left (60%) or right (40%) ATL atrophy. Within ATLs, medial regions are more vulnerable than lateral ones. The observed spectrum of clinical phenotypes is driven by atrophy lateralization. Left and right temporal variants of FTD should be considered the same disease.

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“…In the future, diagnostic help could come from [18F]AV-1451 PET (so called TAU PET) which seems to bind to bilateral 20 temporal lobe pathology in svPPA cases, but does not show frontal/temporal binding in bvFTD (Bevan-Jones et al, 2018;Josephs et al, 2018;Makaretz et al, 2018). However, to date no biomarker for TDP-43 exists (Steinacker, Barschke, & Otto, 2018), so the integration of clinical and neuroimaging findings are still the best way to diagnose these patients. To this end, updating the currently available criteria would be beneficial.…”

Section: Discussionmentioning

confidence: 99%

Regional and hemispheric susceptibility of the temporal lobe to FTLD-TDP type C pathology

Borghesani

Battistella

Mandelli

et al. 2019

Preprint

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410 words Introduction: 1222 words Figures: 5 Tables: 1 Discussion: 2360 words Highlights • Anterior temporal lobe (ATL) degeneration is most often caused by FTLD-TDP-43 type C pathology • Cases can present with predominantly left (60%) or right (40%) ATL atrophy • Within ATLs, medial regions are more vulnerable than lateral ones • Longitudinally, atrophy spreads similarly in predominantly left and right cases • Left and right temporal variants of FTD should be considered the same disease AbstractPost-mortem studies show that focal anterior temporal lobe (ATL) neurodegeneration is most often caused by frontotemporal lobar degeneration TDP-43 type C pathology. Clinically, patients are inconsistently described with the terms semantic variant primary progressive aphasia (svPPA), semantic dementia (SD), or right temporal variant frontotemporal dementia (FTD) depending on whether the predominant symptoms affect language, semantic knowledge for object or people, or socio-emotional behaviors. The neuroimaging hallmark of these syndromes is ATL atrophy, with various degrees of lateralization. Cases presenting with initial right-sided atrophy are considered to be rarer than left-sided ones, yet estimation of their prevalence is hampered by the paucity of studies on wellcharacterized, pathology-proven cohorts. Moreover, it is not clear whether left and right variants show a similar distribution of atrophy within the ATL cross-sectionally and longitudinally.Here we study the largest cohort to-date of pathology-proven TDP-43-C cases diagnosed during life as svPPA, SD or right temporal variant FTD. We analyzed clinical, cognitive, and neuroimaging data from 30 cases, a subset of which was followed longitudinally. Guided by recent structural and functional parcellation studies, we constructed four bilateral ATL regions of interest (ROIs). The computation of an atrophy lateralization index allowed the comparison of atrophy patterns between the two hemispheres. This led to an automatic, imaging-based classification of the cases as left-predominant or right-predominant. We then compared the two groups in terms of regional atrophy patterns within the ATL ROIs (cross-sectionally) and atrophy progression (longitudinally).Results showed that 40% of pathology proven cases diagnosed with a temporal variant presented with right-lateralized atrophy. Moreover, the findings of our ATL ROI analysis indicated that, irrespective of atrophy lateralization, atrophy distribution within both ATLs follows a gradient from medial to lateral regions. Finally, in both left and right cases, atrophy appeared to progress to the contralateral ATL, and from the anterior temporal pole to posterior temporal and orbitofrontal regions.Our results indicate that both left and right predominant ATL atrophy is common in TDP-43-C pathology.Moreover, the distribution of damage within the ATL, as well as its temporal extension, are the same regardless of where the atrophy started. As pharmacological interventions become available, the ability to predict the underlyin...

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Biomarkers for diseases with TDP-43 pathology

Cited by 47 publications

References 236 publications

Limbic-predominant age-related TDP-43 encephalopathy (LATE): consensus working group report

Limbic-predominant age-related TDP-43 encephalopathy (LATE): consensus working group report

Regional and hemispheric susceptibility of the temporal lobe to FTLD-TDP type C pathology

Regional and hemispheric susceptibility of the temporal lobe to FTLD-TDP type C pathology

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