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1 d ARHGAP35 and SERPINA1 with progressive non-fluent aphasia.
2 ontal features and three had progressive non-fluent aphasia.
3 continuous variation within progressive non-fluent aphasia.
4 al aphasia, the two most common kinds of non-fluent aphasia.
5 tical lesion location that gives rise to non-fluent aphasia.
8 atively modality specific in progressive non-fluent aphasia and part of a more severe generic semanti
9 processing occurred in both progressive non-fluent aphasia and semantic dementia, and deficits of se
11 iant FTD, semantic dementia, progressive non-fluent aphasia, and FTD overlapping with motor neuron di
12 All patients developed a progressive non-fluent aphasia culminating in some cases in complete mut
13 analysis were more common in progressive non-fluent aphasia, deficits of apperceptive processing occu
16 impairment that was either a progressive non-fluent aphasia or decreased speech output consistent wit
17 rpersonal functioning, and patients with non-fluent aphasia overestimated emotional and interpersonal
18 c dementia (SD) and six with progressive non-fluent aphasia (PA), as compared to 28 individuals with
19 totemporal dementia (bvFTD), progressive non-fluent aphasia (PNFA) (or a mixed aphasia) and semantic
21 The speech of patients with progressive non-fluent aphasia (PNFA) has often been described clinicall
23 D and the other in a case of progressive non-fluent aphasia (PNFA) without any apparent family histor
24 f ARHGAP35 and SERPINA1 with progressive non-fluent aphasia point towards a potential role of the str
27 ith frontotemporal dementia, progressive non-fluent aphasia, semantic dementia or mixture of these sy
28 a clearer picture of cortical damage in non-fluent aphasia, the current study examined brain damage
30 tia and, with one exception, progressive non-fluent aphasia were associated with transactive response
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