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1
Tractography of supplementary motor area projections in progressive speech apraxia and aphasia
In: Neuroimage Clin (2022)
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2
A molecular pathology, neurobiology, biochemical, genetic and neuroimaging study of progressive apraxia of speech
In: Nat Commun (2021)
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3
Association of amyloid angiopathy with microbleeds in logopenic progressive aphasia: an imaging-pathology study
In: Eur J Neurol (2020)
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4
Longitudinal anatomic, functional, and molecular characterization of Pick disease phenotypes
In: Neurology (2020)
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5
Clinical and Neuroimaging Characteristics of Clinically Unclassifiable Primary Progressive Aphasia
In: Brain Lang (2019)
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6
The influence of β-amyloid on [(18)F]AV-1451 in semantic variant of primary progressive aphasia
Whitwell, Jennifer L.; Martin, Peter R.; Duffy, Joseph R.. - : Lippincott Williams & Wilkins, 2019
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7
[18F]AV-1451 tau-PET and primary progressive aphasia
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8
Tau Uptake in Agrammatic Primary Progressive Aphasia with and without Apraxia of Speech
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9
Disrupted functional connectivity in primary progressive apraxia of speech
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10
Tau-PET imaging with [18F]AV-1451 in Primary Progressive Apraxia of Speech
Abstract: Apraxia of speech is a motor speech disorder characterized by combinations of slow speaking rate, abnormal prosody, distorted sound substitutions, and trial-and-error articulatory movements. Apraxia of speech is due to abnormal planning and/or programming of speech production. It is referred to as primary progressive apraxia of speech (PPAOS) when it is the only symptom of a neurodegenerative condition. Past reports suggest an association of PPAOS with primary 4-repeat (4R) tau (e.g. progressive supranuclear palsy, corticobasal degeneration), rather than amyloid, pathology. The goal of the current study was to investigate the distribution of tau tracer uptake using [18F]AV-1451 positron emission tomography (PET) imaging in patients with PPAOS. Fourteen PPAOS patients underwent [18F]AV-1451 PET (tau-PET) imaging, [C11] Pittsburgh Compound B (PiB) PET and structural MRI and were matched 3:1 by age and sex to 42 cognitively normal controls. Tau-PET uptake was assessed at the region-of-interest (ROI) level and at the voxel-level. The PPAOS group (n=14) showed increased tau-PET uptake in the precentral gyrus, supplementary motor area and Broca’s area compared to controls. To examine whether tau deposition in Broca’s area was related to the presence of aphasia, we examined a subgroup of the PPAOS patients who had predominant apraxia of speech, with concomitant aphasia (PPAOSa; n = 7). The PPAOSa patients showed tau-PET uptake in the same regions as the whole group. However, the remaining seven patients who did not have aphasia showed uptake only in superior premotor and precentral cortices, with no uptake observed in Broca’s area. This cross-sectional study demonstrates that elevated tau tracer uptake is observed using [18F]AV-1451 in PPAOS. Further, it appears that [18F]AV-1451 is sensitive to the regional distribution of tau deposition in different stages of PPAOS, given the relationship between tau signal in Broca’s area and the presence of aphasia.
Keyword: Article
URL: https://doi.org/10.1016/j.cortex.2017.12.021
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5800944/
http://www.ncbi.nlm.nih.gov/pubmed/29353121
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11
Prosodic and Phonetic Subtypes of Primary Progressive Apraxia of Speech
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12
Predicting clinical decline in progressive agrammatic aphasia and apraxia of speech
Whitwell, Jennifer L.; Weigand, Stephen D.; Duffy, Joseph R.. - : Lippincott Williams & Wilkins, 2017
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13
Varying degrees of temporoparietal hypometabolism on FDG-PET reveal amyloid-positive logopenic primary progressive aphasia is not a homogeneous clinical entity
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14
Tracking the Development of Agrammatic Aphasia: a Tensor-Based Morphometry Study
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15
Clinical and MRI models predicting amyloid deposition in progressive aphasia and apraxia of speech
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16
Clinical and neuroimaging biomarkers of amyloid-negative logopenic primary progressive aphasia
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17
Classification and clinicoradiologic features of primary progressive aphasia (PPA) and apraxia of speech
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18
Regional β-amyloid burden does not correlate with cognitive or language deficits in Alzheimer’s disease presenting as aphasia
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19
Progranulin-associated PiB-negative logopenic primary progressive aphasia
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20
Working memory and language network dysfunction in logopenic aphasia: a task-free fMRI comparison to Alzheimer’s dementia
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