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1 diagnosis of FTD (behavioral variant FTD or primary progressive aphasia).
2 ate to syndrome-specific atrophy patterns in primary progressive aphasia.
3 e left language network in logopenic variant primary progressive aphasia.
4 semantic memory deficit in semantic variant primary progressive aphasia.
5 subjects and patients with semantic variant primary progressive aphasia.
6 temporoparietal regions in logopenic variant primary progressive aphasia.
7 (n = 45) and non-fluent (n = 39) variants of primary progressive aphasia.
8 tients represent a fourth variant of 'mixed' primary progressive aphasia.
9 atrophy, making this syndrome distinct from primary progressive aphasia.
10 language tests; hence, none met criteria for primary progressive aphasia.
11 matter changes that occur in the variants of primary progressive aphasia.
12 l in the multimodal diagnostic evaluation of primary progressive aphasia.
13 ed through detailed studies of patients with primary progressive aphasia.
14 nalysis to characterize the heterogeneity of primary progressive aphasia.
15 10 had the non-fluent agrammatic variant of primary progressive aphasia.
16 ical atrophy and eight for logopenic variant primary progressive aphasia.
17 18F-flortaucipir signal in semantic variant primary progressive aphasia.
18 s within language network in each variant of primary progressive aphasia.
19 tributed atrophy pattern in semantic variant primary progressive aphasia.
20 nges in the non-fluent/agrammatic variant of primary progressive aphasia.
21 cits are highly variable in individuals with primary progressive aphasia.
22 seen in most patients with semantic variant primary progressive aphasia.
23 in 43 of type C consistently led to semantic primary progressive aphasia.
24 ropsychological and neuroimaging features of primary progressive aphasia.
25 to verbal fluency and grammar impairment in primary progressive aphasia.
26 t the processing of non-verbal sounds in the primary progressive aphasias.
27 luent (n = 54) and semantic (n = 96) variant primary progressive aphasias.
28 in a consecutive series of 20 patients with primary progressive aphasia [12 with progressive non-flu
29 st common predominant clinical features were primary progressive aphasia (22 patients [25.0%]), behav
30 dementia, 14 patients with semantic variant primary progressive aphasia, 25 patients with Alzheimer'
31 hy, 4 subjects with the logopenic variant of primary progressive aphasia, 6 age-matched patients with
33 striking gains of function in a patient with primary progressive aphasia, a degenerative disease of t
34 work is affected in the nonfluent variant of primary progressive aphasia, a neurodegenerative disorde
35 Eight patients with the nonfluent variant of primary progressive aphasia (age, 67.0 +/- 7.4 y; 4 wome
37 (behavioral variant, semantic and non-fluent primary progressive aphasia) along with associated three
38 analysed speech samples for 50 patients with primary progressive aphasia, along with neurodegenerativ
40 frontotemporal dementia and semantic variant primary progressive aphasia (also called semantic dement
42 (behavioral variant frontotemporal dementia, primary progressive aphasias, Alzheimer's disease, Parki
43 eed region derived from the semantic variant primary progressive aphasia analysis was strongly connec
44 ral dementia, 10 had the semantic variant of primary progressive aphasia and 10 had the non-fluent ag
45 tions on 28 TDP-C patients, 18 with semantic primary progressive aphasia and 10 with other syndromes.
46 5 years), 12 patients with logopenic variant primary progressive aphasia and 13 patients with posteri
48 We asked 15 patients with semantic variant primary progressive aphasia and 57 patients with Alzheim
49 playing AD with severe language problems and primary progressive aphasia and a near splice-site mutat
50 frontotemporal dementia or semantic variant primary progressive aphasia and a structural MRI (n = 47
54 temporal regions, and both semantic variant primary progressive aphasia and behavioural variant fron
56 t tract underlies verbal fluency deficits in primary progressive aphasia and further confirm the role
58 icits and meet criteria for semantic variant primary progressive aphasia and semantic dementia, patie
60 l-variant FTD, non-fluent/agrammatic variant primary progressive aphasia and semantic variant PPA.
61 n-verbal sound perception and recognition in primary progressive aphasia and specific disorders at pe
62 ns of linguistic assessments in the study of primary progressive aphasia and the three most prevalent
63 rior cortical atrophy than logopenic variant primary progressive aphasia) and higher-order visual net
64 bvFTD), 89 patients with semantic variant of primary progressive aphasia, and 30 patients with Huntin
65 tia, semantic variant and non-fluent variant primary progressive aphasia, and 46 healthy controls) de
66 89 patients (27.0%) with semantic variant of primary progressive aphasia, and 6 of 30 patients (20%)
67 osterior cortical atrophy, logopenic variant primary progressive aphasia, and corticobasal syndrome).
68 cognitive difficulties in logopenic variant primary progressive aphasia, and predicts phenotypic div
69 fluent (n = 34) or semantic (n = 37) variant primary progressive aphasia-and 100 cognitively normal i
71 gh some phenotypes such as logopenic variant primary progressive aphasia are more commonly associated
76 re the evolution of the logopenic variant of primary progressive aphasia as a distinct clinical entit
77 istered to one patient with semantic variant primary progressive aphasia before repeating 18F-flortau
78 ening the understanding of logopenic variant primary progressive aphasia beyond the lens of an exclus
79 ed greater leftward asymmetry for tangles in primary progressive aphasia but not in the amnestic Alzh
80 : emotion recognition in semantic variant of primary progressive aphasia', by Bertoux et al. (doi:10.
81 nnected speech production in each variant of primary progressive aphasia, by quantifying speech outpu
84 nships are not universal and that individual primary progressive aphasia cases with Alzheimer patholo
85 rnia San Francisco Memory and Aging Center's primary progressive aphasia cohort (n = 198) for history
86 51 binding was increased in semantic variant primary progressive aphasia compared to controls in the
87 imary progressive aphasia; logopenic variant primary progressive aphasia), compared to 25 healthy age
88 ntactic comprehension in 51 individuals with primary progressive aphasia, composed of all clinical va
89 specific syndromes (Alzheimer's disease and primary progressive aphasia) converge over time into a d
90 diagnoses included frontotemporal dementia, primary progressive aphasia, corticobasal syndrome, and
91 tudy, leveraging machine learning on a large primary progressive aphasia dataset, delineated four dis
92 ortical atrophy and the logopenic variant of primary progressive aphasia, differ from amnestic AD in
93 0.001), while patients with semantic variant primary progressive aphasia discounted delayed rewards m
95 in a consecutive series of 18 patients with primary progressive aphasia (eight with semantic variant
96 er neocortical-to-entorhinal tangle ratio in primary progressive aphasia establishes clinical concord
97 corticobasal syndrome, and nonfluent-variant primary progressive aphasia) exhibited higher globus pal
98 9 (7.0) years], nine with non-fluent variant primary progressive aphasia [five female; 67.4 (8.1) yea
99 sive aphasia (nonfluent PPA; n = 15), fluent primary progressive aphasia (fluent PPA; n = 7), and amy
100 a core central auditory impairment exists in primary progressive aphasia for non-linguistic stimuli.
101 64.8 (6.8) years], 12 with semantic variant primary progressive aphasia [four female; 66.9 (7.0) yea
102 different to that seen in the fluent form of primary progressive aphasia (fPPA), a neurodegenerative
103 ion deficits, helping to dissociate semantic primary progressive aphasia from semantic dementia.
104 s for distinguishing the semantic variant of primary progressive aphasia from the partially overlappi
105 Moreover, patients with semantic variant primary progressive aphasia had a significantly more pro
107 follow-up, all participants with non-fluent primary progressive aphasia had evolved either corticoba
110 ment before making a definitive diagnosis of primary progressive aphasia has promoted diagnostic spec
113 s been associated with syntactic deficits in primary progressive aphasia in a number of structural an
114 co-pathological relationships in subtypes of primary progressive aphasia in hopes of utilizing langua
117 Patient presenting with logopenic variant primary progressive aphasia initially thought to be due
126 irment for natural kinds in semantic variant primary progressive aphasia is related in part to diseas
127 discovered four neuroanatomical subtypes of primary progressive aphasia, labelled S1 (left temporal)
128 y and executive deficits), logopenic variant primary progressive aphasia (language deficits), and pos
130 rimary progressive aphasia; semantic variant primary progressive aphasia; logopenic variant primary p
131 Most subjects with logopenic variant of primary progressive aphasia (lvPPA) have beta-amyloid (A
132 n participants with the logopenic variant of primary progressive aphasia (lvPPA) performed a recognit
133 sterior cortical atrophy (PCA), 12 logopenic primary progressive aphasia (lvPPA), 20 behavioural vari
134 al atrophy/PCA-AD; n = 103 logopenic variant primary progressive aphasia/lvPPA-AD; n = 35 behavioural
135 st that cortical atrophy in semantic variant primary progressive aphasia may follow connectional path
136 Cortical Atrophy (n = 16); logopenic variant Primary Progressive Aphasia (n = 15); and amnestic syndr
138 nestic variants, including logopenic-variant primary progressive aphasia (n = 25), posterior cortical
139 's disease, semantic dementia and non-fluent primary progressive aphasia (n = 9 each) were contrasted
140 Disease Research Center (semantic variant of primary progressive aphasia, n = 7; behavioural variant
141 ndrome, n = 13; behavioural variant, n = 14; primary progressive aphasias, n = 21) and 27 control sub
143 ture of the non-fluent/agrammatic variant of primary progressive aphasia (naPPA), but well-controlled
144 al dementia (bvFTD n=64), non-fluent variant primary progressive aphasia (nfvPPA n=36), semantic vari
145 ssive aphasia (svPPA), 14 non-fluent variant primary progressive aphasia (nfvPPA) and 12 semantic beh
146 the biomarker cascades in non-fluent variant primary progressive aphasia (nfvPPA) and behavioural var
147 hology in patients with nonfluent/agrammatic primary progressive aphasia (nfvPPA) and progressive sup
149 sive aphasia (svPPA), (4) non-fluent variant primary progressive aphasia (nfvPPA) or (5) early onset
150 phasia (svPPA), five with non-fluent variant primary progressive aphasia (nfvPPA)) and 17 healthy con
151 ionally termed non-fluent/agrammatic variant primary progressive aphasia (nfvPPA), or exist as two co
152 temporal dementia (bvFTD), nonfluent variant primary progressive aphasia (nfvPPA), posterior cortical
153 y Richardson syndrome (PSP-RS) and nonfluent primary progressive aphasia (nfvPPA), where underlying f
154 epresenting the three canonical syndromes of primary progressive aphasia (non-fluent/agrammatic varia
155 ed in difficulty, in patients with nonfluent primary progressive aphasia (nonfluent PPA; n = 15), flu
156 sed on larger groups of patients with either primary progressive aphasia or a typical amnestic dement
157 only associated with the semantic variant of primary progressive aphasia or behavioural variant front
159 pe, posterior cortical atrophy, or logopenic primary progressive aphasia), or MCI with uncommon AD or
160 ary progressive aphasia, or semantic variant primary progressive aphasia), or mild cognitive impairme
161 heimer's disease dementia, logopenic variant primary progressive aphasia, or posterior cortical atrop
162 frontotemporal dementia, non-fluent variant primary progressive aphasia, or semantic variant primary
163 frontotemporal dementia and semantic variant primary progressive aphasia patients alone confirmed thi
164 corticobasal syndrome, and nonfluent-variant primary progressive aphasia patients had a pallidal SUVr
165 se, non-fluent variant and logopenic variant primary progressive aphasia patients very well from heal
166 odulated to a lesser extent or not at all in primary progressive aphasia patients whose syntax was re
168 tly limbic and symmetric pathology cause the primary progressive aphasia phenotype, characterized by
169 ral variant frontotemporal dementia (bvFTD), primary progressive aphasia (PPA) and corticobasal syndr
170 ral language productions of individuals with primary progressive aphasia (PPA) and healthy individual
171 usions) have been described in patients with primary progressive aphasia (PPA) but their diagnostic v
188 diagnosis in a large cohort of patients with primary progressive aphasia (PPA) variants defined by cu
189 sia when predominantly right-sided, semantic Primary Progressive Aphasia (PPA) when left-sided, and s
190 aging, and genetic study of 31 patients with primary progressive aphasia (PPA), a decline in language
192 autopsy in up to one third of patients with primary progressive aphasia (PPA), but clinical features
194 essionals in the management and treatment of primary progressive aphasia (PPA), however, there are ga
195 D), amyotrophic lateral sclerosis (ALS), and primary progressive aphasia (PPA), including 281 AD, 256
196 mentia, non-fluent, and semantic variants of primary progressive aphasia (PPA), progressive supranucl
198 the nonfluent variant or semantic variant of primary progressive aphasia (PPA), unspecified PPA, prog
203 eurodegenerative dementia syndromes, such as primary progressive aphasias (PPA), have traditionally b
204 -stroke aphasia, PSA) and neurodegeneration (primary progressive aphasia, PPA) have overlapping sympt
205 n 118 consecutive autopsies on patients with primary progressive aphasia, primary diagnosis was Alzhe
206 eration and resultant language impairment in primary progressive aphasia reflect complex interactions
207 est that syntactic comprehension deficits in primary progressive aphasia reflect not only structural
208 t language network for the logopenic variant primary progressive aphasia region of interest, and the
209 sion in the non-fluent/agrammatic variant of primary progressive aphasia relates to the strength of c
212 Our study included 270 participants with primary progressive aphasia seen for research in the UCL
213 ssive aphasia (non-fluent/agrammatic variant primary progressive aphasia; semantic variant primary pr
214 the pathological process in semantic variant primary progressive aphasia, should be further studied a
215 uroanatomical phenotypes do exist within the primary progressive aphasia spectrum, but that these are
216 of atrophy in non-fluent/agrammatic variant primary progressive aphasia spreads over time from a syn
217 p that was matched in age and gender to each primary progressive aphasia subgroup (n = 20, age = 65 +
221 stic cognitive deficits in logopenic variant primary progressive aphasia, suggesting that degeneratio
222 sive aphasia (nfvPPA n=36), semantic variant primary progressive aphasia (svPPA n=25), progressive su
225 al dementia (rtFTD), (3) semantic variant of primary progressive aphasia (svPPA), (4) non-fluent vari
226 ral variant FTD (bvFTD), 13 semantic variant primary progressive aphasia (svPPA), 14 non-fluent varia
227 l lobe (ATL): patients with semantic variant primary progressive aphasia (svPPA), a clinical syndrome
228 ementia (bvFTD), eight with semantic variant primary progressive aphasia (svPPA), five with non-fluen
229 dementia, including the semantic variant of primary progressive aphasia (svPPA), is strongly associa
234 patients with bvFTD and semantic variant of primary progressive aphasia than in those with AD and is
235 in Alzheimer's disease and logopenic variant primary progressive aphasia than semantic variant primar
236 nition of this area and presenting data from primary progressive aphasia that challenged this classic
238 operculum and caudate nucleus in non-fluent primary progressive aphasia (the corticobasal degenerati
239 ltiple clinical subtypes, and one subtype of primary progressive aphasia to be caused by multiple neu
241 yses related performance in semantic variant primary progressive aphasia to ventral and medial portio
242 h semantic dementia (SD) or semantic variant primary progressive aphasia typically present with marke
243 -PET-negative patients with semantic variant primary progressive aphasia underwent 11C-PBR28 and 18F-
244 istent region of atrophy in semantic variant primary progressive aphasia using cortical thickness ana
245 pography of inflammation in semantic variant primary progressive aphasia using high-resolution PET an
246 mage and syntactic deficits in patients with primary progressive aphasia, using multimodal neuroimagi
248 s of regional spectral power changes in each primary progressive aphasia variant, compared to age-mat
252 ntre of the non-fluent/agrammatic variant of primary progressive aphasia was derived in a group of 10
254 feature for all pathologies associated with primary progressive aphasia was the asymmetric prominenc
256 ical diagnosis of frontotemporal dementia or primary progressive aphasia, we included 70 subjects wit
257 -linguistic dysfunction in logopenic variant primary progressive aphasia, we propose that a significa
258 frontotemporal dementia and semantic variant primary progressive aphasia were most likely to exhibit
259 sis of patients with the semantic subtype of primary progressive aphasia, which is associated with ma
260 ntroversy were addressed in 72 patients with primary progressive aphasia who collectively displayed a
261 fied clinically into behavioral variant FTD; primary progressive aphasia with 3 subtypes, semantic, n
263 ing research has associated semantic variant primary progressive aphasia with distributed cortical at
265 ing in healthy controls and in patients with primary progressive aphasia with relatively spared synta
266 et Alzheimer's disease and logopenic variant primary progressive aphasia), with a trend towards lower
267 thology displays an atypical distribution in primary progressive aphasia yielded inconclusive results