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1 s within language network in each variant of primary progressive aphasia.
2 temporoparietal regions in logopenic variant primary progressive aphasia.
3 tients represent a fourth variant of 'mixed' primary progressive aphasia.
4 atrophy, making this syndrome distinct from primary progressive aphasia.
5 language tests; hence, none met criteria for primary progressive aphasia.
6 matter changes that occur in the variants of primary progressive aphasia.
7 l in the multimodal diagnostic evaluation of primary progressive aphasia.
8 ed through detailed studies of patients with primary progressive aphasia.
9 tributed atrophy pattern in semantic variant primary progressive aphasia.
10 nges in the non-fluent/agrammatic variant of primary progressive aphasia.
11 ical atrophy and eight for logopenic variant primary progressive aphasia.
12 cits are highly variable in individuals with primary progressive aphasia.
13 seen in most patients with semantic variant primary progressive aphasia.
14 in 43 of type C consistently led to semantic primary progressive aphasia.
15 ropsychological and neuroimaging features of primary progressive aphasia.
16 to verbal fluency and grammar impairment in primary progressive aphasia.
17 e left language network in logopenic variant primary progressive aphasia.
18 semantic memory deficit in semantic variant primary progressive aphasia.
19 subjects and patients with semantic variant primary progressive aphasia.
20 t the processing of non-verbal sounds in the primary progressive aphasias.
21 luent (n = 54) and semantic (n = 96) variant primary progressive aphasias.
22 in a consecutive series of 20 patients with primary progressive aphasia [12 with progressive non-flu
23 dementia, 14 patients with semantic variant primary progressive aphasia, 25 patients with Alzheimer'
24 hy, 4 subjects with the logopenic variant of primary progressive aphasia, 6 age-matched patients with
26 striking gains of function in a patient with primary progressive aphasia, a degenerative disease of t
27 analysed speech samples for 50 patients with primary progressive aphasia, along with neurodegenerativ
29 frontotemporal dementia and semantic variant primary progressive aphasia (also called semantic dement
31 eed region derived from the semantic variant primary progressive aphasia analysis was strongly connec
32 5 years), 12 patients with logopenic variant primary progressive aphasia and 13 patients with posteri
34 We asked 15 patients with semantic variant primary progressive aphasia and 57 patients with Alzheim
39 t tract underlies verbal fluency deficits in primary progressive aphasia and further confirm the role
41 n-verbal sound perception and recognition in primary progressive aphasia and specific disorders at pe
42 rior cortical atrophy than logopenic variant primary progressive aphasia) and higher-order visual net
43 bvFTD), 89 patients with semantic variant of primary progressive aphasia, and 30 patients with Huntin
44 tia, semantic variant and non-fluent variant primary progressive aphasia, and 46 healthy controls) de
45 89 patients (27.0%) with semantic variant of primary progressive aphasia, and 6 of 30 patients (20%)
46 osterior cortical atrophy, logopenic variant primary progressive aphasia, and corticobasal syndrome).
51 re the evolution of the logopenic variant of primary progressive aphasia as a distinct clinical entit
52 ed greater leftward asymmetry for tangles in primary progressive aphasia but not in the amnestic Alzh
53 nnected speech production in each variant of primary progressive aphasia, by quantifying speech outpu
55 nships are not universal and that individual primary progressive aphasia cases with Alzheimer patholo
56 rnia San Francisco Memory and Aging Center's primary progressive aphasia cohort (n = 198) for history
57 ntactic comprehension in 51 individuals with primary progressive aphasia, composed of all clinical va
58 diagnoses included frontotemporal dementia, primary progressive aphasia, corticobasal syndrome, and
59 ortical atrophy and the logopenic variant of primary progressive aphasia, differ from amnestic AD in
60 0.001), while patients with semantic variant primary progressive aphasia discounted delayed rewards m
62 in a consecutive series of 18 patients with primary progressive aphasia (eight with semantic variant
63 er neocortical-to-entorhinal tangle ratio in primary progressive aphasia establishes clinical concord
64 sive aphasia (nonfluent PPA; n = 15), fluent primary progressive aphasia (fluent PPA; n = 7), and amy
65 a core central auditory impairment exists in primary progressive aphasia for non-linguistic stimuli.
66 different to that seen in the fluent form of primary progressive aphasia (fPPA), a neurodegenerative
67 s for distinguishing the semantic variant of primary progressive aphasia from the partially overlappi
68 Moreover, patients with semantic variant primary progressive aphasia had a significantly more pro
70 follow-up, all participants with non-fluent primary progressive aphasia had evolved either corticoba
73 ment before making a definitive diagnosis of primary progressive aphasia has promoted diagnostic spec
76 s been associated with syntactic deficits in primary progressive aphasia in a number of structural an
77 co-pathological relationships in subtypes of primary progressive aphasia in hopes of utilizing langua
79 Patient presenting with logopenic variant primary progressive aphasia initially thought to be due
86 irment for natural kinds in semantic variant primary progressive aphasia is related in part to diseas
87 y and executive deficits), logopenic variant primary progressive aphasia (language deficits), and pos
90 n participants with the logopenic variant of primary progressive aphasia (lvPPA) performed a recognit
91 sterior cortical atrophy (PCA), 12 logopenic primary progressive aphasia (lvPPA), 20 behavioural vari
92 st that cortical atrophy in semantic variant primary progressive aphasia may follow connectional path
93 's disease, semantic dementia and non-fluent primary progressive aphasia (n = 9 each) were contrasted
94 ndrome, n = 13; behavioural variant, n = 14; primary progressive aphasias, n = 21) and 27 control sub
96 ture of the non-fluent/agrammatic variant of primary progressive aphasia (naPPA), but well-controlled
97 hology in patients with nonfluent/agrammatic primary progressive aphasia (nfvPPA) and progressive sup
98 sive aphasia (svPPA), (4) non-fluent variant primary progressive aphasia (nfvPPA) or (5) early onset
99 phasia (svPPA), five with non-fluent variant primary progressive aphasia (nfvPPA)) and 17 healthy con
100 ed in difficulty, in patients with nonfluent primary progressive aphasia (nonfluent PPA; n = 15), flu
101 sed on larger groups of patients with either primary progressive aphasia or a typical amnestic dement
103 frontotemporal dementia and semantic variant primary progressive aphasia patients alone confirmed thi
104 odulated to a lesser extent or not at all in primary progressive aphasia patients whose syntax was re
105 tly limbic and symmetric pathology cause the primary progressive aphasia phenotype, characterized by
106 ral variant frontotemporal dementia (bvFTD), primary progressive aphasia (PPA) and corticobasal syndr
120 diagnosis in a large cohort of patients with primary progressive aphasia (PPA) variants defined by cu
121 aging, and genetic study of 31 patients with primary progressive aphasia (PPA), a decline in language
123 autopsy in up to one third of patients with primary progressive aphasia (PPA), but clinical features
125 D), amyotrophic lateral sclerosis (ALS), and primary progressive aphasia (PPA), including 281 AD, 256
129 est that syntactic comprehension deficits in primary progressive aphasia reflect not only structural
130 t language network for the logopenic variant primary progressive aphasia region of interest, and the
131 sion in the non-fluent/agrammatic variant of primary progressive aphasia relates to the strength of c
133 of atrophy in non-fluent/agrammatic variant primary progressive aphasia spreads over time from a syn
134 p that was matched in age and gender to each primary progressive aphasia subgroup (n = 20, age = 65 +
138 al dementia (rtFTD), (3) semantic variant of primary progressive aphasia (svPPA), (4) non-fluent vari
139 ementia (bvFTD), eight with semantic variant primary progressive aphasia (svPPA), five with non-fluen
140 dementia, including the semantic variant of primary progressive aphasia (svPPA), is strongly associa
142 patients with bvFTD and semantic variant of primary progressive aphasia than in those with AD and is
144 operculum and caudate nucleus in non-fluent primary progressive aphasia (the corticobasal degenerati
146 yses related performance in semantic variant primary progressive aphasia to ventral and medial portio
147 istent region of atrophy in semantic variant primary progressive aphasia using cortical thickness ana
148 mage and syntactic deficits in patients with primary progressive aphasia, using multimodal neuroimagi
149 s of regional spectral power changes in each primary progressive aphasia variant, compared to age-mat
153 ntre of the non-fluent/agrammatic variant of primary progressive aphasia was derived in a group of 10
155 feature for all pathologies associated with primary progressive aphasia was the asymmetric prominenc
156 frontotemporal dementia and semantic variant primary progressive aphasia were most likely to exhibit
157 sis of patients with the semantic subtype of primary progressive aphasia, which is associated with ma
158 ntroversy were addressed in 72 patients with primary progressive aphasia who collectively displayed a
160 ing research has associated semantic variant primary progressive aphasia with distributed cortical at
162 ing in healthy controls and in patients with primary progressive aphasia with relatively spared synta
163 et Alzheimer's disease and logopenic variant primary progressive aphasia), with a trend towards lower
164 thology displays an atypical distribution in primary progressive aphasia yielded inconclusive results
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