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1 er's disease, dementia with Lewy bodies, and progressive supranuclear palsy).
2 s (22% in multiple system atrophy and 50% in progressive supranuclear palsy).
3 ad primary co-morbid FTD-spectrum pathology (progressive supranuclear palsy).
4 sease, to relatively little loss, as seen in progressive supranuclear palsy.
5 those managing and caring for patients with progressive supranuclear palsy.
6 a model to examine brainstem pathogenesis of progressive supranuclear palsy.
7 e pathology in corticobasal degeneration and progressive supranuclear palsy.
8 s for the treatment of Alzheimer disease and progressive supranuclear palsy.
9 other neurodegenerative diseases, including progressive supranuclear palsy.
10 cluding Alzheimer disease, Pick disease, and progressive supranuclear palsy.
11 milar to those of multiple system atrophy or progressive supranuclear palsy.
12 nson's disease, multiple system atrophy, and progressive supranuclear palsy.
13 n that SNP6 is also associated with risk for progressive supranuclear palsy.
14 formation of NFTs in Alzheimer's disease and progressive supranuclear palsy.
15 cal and pathological characteristics such as progressive supranuclear palsy.
16 tion shares a common genetic background with progressive supranuclear palsy.
17 arate disorder or a spectrum of disease with progressive supranuclear palsy.
18 with a distribution similar to that found in progressive supranuclear palsy.
19 l degeneration, and Parkinson's disease with progressive supranuclear palsy.
20 ated tau pathology, but less specifically in progressive supranuclear palsy.
21 y, especially in primary tauopathies such as progressive supranuclear palsy.
22 e extent for cortico basal syndrome, but not progressive supranuclear palsy.
23 tem atrophy, and in all regions examined for progressive supranuclear palsy.
24 nson's disease, multiple system atrophy, and progressive supranuclear palsy.
26 were CBD (35%), Alzheimer disease (AD, 23%), progressive supranuclear palsy (13%), and frontotemporal
28 thods: Fifteen subjects (4 controls, 6 AD, 3 progressive supranuclear palsy, 2 cortico basal syndrome
31 hasia [PNFA], 16 semantic dementia [SD]), 22 progressive supranuclear palsy, 50 Alzheimer disease, 6
32 , 96% specificity, 97% PPV, and 83% NPV) and progressive supranuclear palsy (88% sensitivity, 94% spe
33 ecificity (corticobasal degeneration: 92.7%; progressive supranuclear palsy: 94.1%) in classifying 58
34 tter lesion in corticobasal degeneration and progressive supranuclear palsy-a pathologically proven f
35 egeneration had been clinically diagnosed as progressive supranuclear palsy, all of whom had vertical
36 and the neuropathologic phenotype resembles progressive supranuclear palsy, an alternative considera
37 pt size, was present in 75% of patients with progressive supranuclear palsy and 15% of patients with
38 rment was observed in 62.0% of patients with progressive supranuclear palsy and 31.8% of those with m
39 om patients with AD, Parkinson's disease, or progressive supranuclear palsy and control subjects seen
40 rofibrillary tangles in Alzheimer's disease, progressive supranuclear palsy and corticobasal degenera
41 nks FTD to other forms of tauopathy, such as progressive supranuclear palsy and corticobasal degenera
42 ementia with Lewy bodies but is not found in progressive supranuclear palsy and corticobasal degenera
43 tive diseases including Alzheimer's disease, progressive supranuclear palsy and corticobasal degenera
44 pear to be genetic risk factors for sporadic progressive supranuclear palsy and corticobasal degenera
46 between individual patients using 1H-MRSI in progressive supranuclear palsy and corticobasal degenera
47 nal pattern of neuronal involvement found in progressive supranuclear palsy and corticobasal degenera
48 pecific binding was, however, found on human progressive supranuclear palsy and corticobasal degenera
49 temporal lobar degeneration, Pick's disease, progressive supranuclear palsy and corticobasal degenera
50 other tauopathies including Pick's disease, progressive supranuclear palsy and corticobasal degenera
51 anguage variants of frontotemporal dementia, progressive supranuclear palsy and corticobasal syndrome
52 of modality-independent social cognition in progressive supranuclear palsy and explore the neural co
53 We have recently examined the MAPT locus in progressive supranuclear palsy and found that a haplotyp
54 ous to the tau haplotype over-represented in progressive supranuclear palsy and further extend the si
55 spectively recruited cohort of patients with progressive supranuclear palsy and multiple system atrop
56 tudy identified new genetic risk factors for progressive supranuclear palsy and new genetic condition
57 the clinical and pathologic overlap between progressive supranuclear palsy and other disorders remai
59 nson's disease, multiple system atrophy, and progressive supranuclear palsy and to accurately disting
60 dividuals presented with an atypical form of progressive supranuclear palsy and two others with eithe
61 zheimer's disease, relative to patients with progressive supranuclear palsy and with control subjects
62 he testes syndrome), a rare complex disease (progressive supranuclear palsy), and a common complex di
63 mild cognitive impairment), 19 patients with progressive supranuclear palsy, and 13 age- and sex-matc
64 with corticobasal syndrome, 31 patients with progressive supranuclear palsy, and 222 control subjects
65 ssue from patients with Alzheimer's disease, progressive supranuclear palsy, and a control case to as
66 ive diseases, including Alzheimer's disease, progressive supranuclear palsy, and cases of frontotempo
67 ia and parkinsonism linked to chromosome 17, progressive supranuclear palsy, and corticobasal degener
68 yndromes, including multiple-system atrophy, progressive supranuclear palsy, and corticobasal degener
69 ics were determined for Alzheimer's disease, progressive supranuclear palsy, and corticobasal degener
70 PET for diagnosing multiple-system atrophy, progressive supranuclear palsy, and corticobasal degener
71 n disease, chronic traumatic encephalopathy, progressive supranuclear palsy, and corticobasal degener
72 k disease, argyrophilic grain disease (AGD), progressive supranuclear palsy, and corticobasal degener
73 ified by sporadic corticobasal degeneration, progressive supranuclear palsy, and Pick's disease, as w
75 oral dementia, corticobasal degeneration and progressive supranuclear palsy, are characterized by agg
76 F pattern compared with the 13 patients with progressive supranuclear palsy (baseline area under the
77 subjects, while both Parkinson's disease and progressive supranuclear palsy brains showed marked depl
78 evel of cognitive impairment associated with progressive supranuclear palsy, but also point to compar
79 ntia nigra, both multiple system atrophy and progressive supranuclear palsy, but not Parkinson's dise
81 with the Richardson syndrome presentation of progressive supranuclear palsy, characterized by postura
82 urodegeneration causing Alzheimer's disease, progressive supranuclear palsy, chronic traumatic enceph
83 tiple neurodegenerative disorders, including progressive supranuclear palsy, corticobasal degeneratio
84 mortem human brain tissue from Pick disease, progressive supranuclear palsy, corticobasal degeneratio
85 with four-repeat (4R) tauopathies, including progressive supranuclear palsy, corticobasal degeneratio
86 basal ganglia disorders (Parkinson disease, progressive supranuclear palsy, corticobasal degeneratio
87 dementing disorders, such as Pick's disease, progressive supranuclear palsy, corticobasal degeneratio
88 comprised of 4-repeat isoforms in brains of progressive supranuclear palsy, corticobasal degeneratio
89 ve response DNA binding protein 43 (TDP-43), progressive supranuclear palsy, corticobasal degeneratio
91 f Neurological Disorders and the Society for Progressive Supranuclear Palsy) diagnostic criteria for
93 D-tau (34 10 corticobasal degeneration, nine progressive supranuclear palsy, eight Pick's disease, th
94 ry patient with corticobasal degeneration or progressive supranuclear palsy fell outside 95% of the n
96 ent was observed in approximately 57% of the progressive supranuclear palsy group and 20% of the mult
97 dentified in 87% of finger tap trials in the progressive supranuclear palsy group and only 12% in the
102 drome, it is not known whether patients with progressive supranuclear palsy have criteria-defined bra
103 isorders such as multiple system atrophy and progressive supranuclear palsy have elevated free-water
104 pe) and three forms of subcortical dementia (progressive supranuclear palsy, Huntington's and Parkins
105 differentiate corticobasal degeneration from progressive supranuclear palsy in patients with Richards
106 n the putamen and caudate, and increased for progressive supranuclear palsy in the putamen, caudate,
107 of tau pathology in Alzheimer's disease and progressive supranuclear palsy in vivo would help to dev
108 indicate that corticobasal degeneration and progressive supranuclear palsy, in particular, might be
112 ill rapidly evolve and develop a devastating progressive supranuclear palsy-like syndrome approximate
113 gression of symptoms that had evolved into a progressive supranuclear palsy-like syndrome; they showe
114 disease (AD), corticobasal degeneration, and progressive supranuclear palsy, likely representing a ma
117 patients with Parkinson's disease (n = 15), progressive supranuclear palsy (n = 9) and healthy age-
118 of either multiple system atrophy (n=372) or progressive supranuclear palsy (n=311) from the Neuropro
119 and white matter in a subset of 70 patients (progressive supranuclear palsy, n = 22; corticobasal syn
120 igra compared to control tissue, and also in progressive supranuclear palsy nigra, but not Parkinson'
121 syndrome is a rare clinical presentation of progressive supranuclear palsy occurring in only 6 of th
122 linical picture closely resembling classical progressive supranuclear palsy or Richardson's syndrome,
123 panded ATXN2 repeats with the development of progressive supranuclear palsy (OR = 5.83; P= 0.004; rep
124 such tauopathies as frontotemporal dementia, progressive supranuclear palsy, or Alzheimer's disease.
125 from PD cases but not in Alzheimer disease, progressive supranuclear palsy, or multiple system atrop
126 ical and subcortical neuronal involvement in progressive supranuclear palsy, Parkinson's disease and
127 and synucleinopathies: Alzheimer's disease, progressive supranuclear palsy, Parkinson's disease, dem
128 supranuclear palsy-tau pathology now include progressive supranuclear palsy-parkinsonism (PSP-P), in
129 ve predictive value of 23.8%; six others had progressive supranuclear palsy pathology, five had Alzhe
132 usting for the possible misclassification of progressive supranuclear palsy patients as Parkinson's d
133 Factors that may contribute toward managing progressive supranuclear palsy patients better are discu
134 ot detected in any corticobasal syndrome and progressive supranuclear palsy patients or controls.
137 generation cases presented clinically with a progressive supranuclear palsy phenotype and 29% of case
139 latively uncommon neurodegenerative diseases-progressive supranuclear palsy, Pick's disease, and cort
140 f glial and neuronal tau pathologies in CBD, progressive supranuclear palsy, PiD, and frontotemporal
141 ansgenic mice partly resembled those seen in progressive supranuclear palsy, presenting these animals
142 multiple system atrophy (P < 0.001) but not progressive supranuclear palsy, presumably because of th
143 and 50 controls from the PIck's disease and Progressive supranuclear palsy Prevalence and INcidence
144 II) developed a movement disorder resembling progressive supranuclear palsy (PSP) and associated with
145 ic feature of the neurodegenerative diseases progressive supranuclear palsy (PSP) and corticobasal de
146 type H1 is over-represented in patients with progressive supranuclear palsy (PSP) and corticobasal de
148 ent in Alzheimer disease (AD), Pick disease, progressive supranuclear palsy (PSP) and corticobasal de
151 a-spectrum (FTD-s) disorders, including FTD, progressive supranuclear palsy (PSP) and corticobasal sy
152 says to include a limited number of cases of progressive supranuclear palsy (PSP) and dementia with L
153 ies, which include Alzheimer's disease (AD), progressive supranuclear palsy (PSP) and frontotemporal
154 gnostic predictors have not been defined for progressive supranuclear palsy (PSP) and multiple system
155 ationship to clinical disease progression in progressive supranuclear palsy (PSP) and multiple system
156 nostic factors and survival in patients with progressive supranuclear palsy (PSP) and multiple system
159 nts with corticobasal degeneration (CBD) and progressive supranuclear palsy (PSP) can sometimes prese
160 rements in postmortem brain samples from two progressive supranuclear palsy (PSP) cases and a MAPT P3
161 alleles were excessively represented in the progressive supranuclear palsy (PSP) group, compared wit
162 Testing for association of CBD with top progressive supranuclear palsy (PSP) GWAS single-nucleot
166 udies assessing binding to tau aggregates in progressive supranuclear palsy (PSP) have yielded mixed
167 a study to estimate the point prevalence of progressive supranuclear palsy (PSP) in the UK at nation
174 PD compared with patients with diagnoses of progressive supranuclear palsy (PSP) or Alzheimer's dise
175 tic primary progressive aphasia (nfvPPA) and progressive supranuclear palsy (PSP) or corticobasal deg
179 systems in multiple-system atrophy (MSA) and progressive supranuclear palsy (PSP) than in Parkinson d
180 agnosis of multiple system atrophy (MSA) and progressive supranuclear palsy (PSP) were 85.7 (30 out o
181 occurs in multiple system atrophy (MSA) and progressive supranuclear palsy (PSP) where nigral dopami
182 idiopathic Parkinson's disease (PD), 30 with progressive supranuclear palsy (PSP), 19 with corticobas
183 ariety of neurological conditions, including progressive supranuclear palsy (PSP), a late-onset atypi
184 auopathy with prominent Abeta pathology, and progressive supranuclear palsy (PSP), a primary tauopath
186 le system atrophy (MSA), pure akinesia (PA), progressive supranuclear palsy (PSP), and cortical-basal
187 sorders, including Alzheimer's disease (AD), progressive supranuclear palsy (PSP), and frontotemporal
188 pical and atypical, pathologically diagnosed progressive supranuclear palsy (PSP), and investigated t
189 ncluding corticobasal degeneration (CBD) and progressive supranuclear palsy (PSP), are neurodegenerat
190 nically with corticobasal syndrome (CBS) and progressive supranuclear palsy (PSP), both of which have
191 nificantly over-represented in patients with progressive supranuclear palsy (PSP), extending earlier
192 ypical parkinsonian syndromes (APSs) such as progressive supranuclear palsy (PSP), multiple system at
196 (IPD) from multiple system atrophy (MSA) and progressive supranuclear palsy (PSP), the most common at
206 n = 14), Huntington's disease (HD, n = 11), progressive supranuclear palsy (PSP, n = 11), young adul
208 acted from postmortem brains of AD (AD-tau), progressive supranuclear palsy (PSP-tau), and corticobas
209 = 30), Parkinson's disease (PD; n = 32), and progressive supranuclear palsy (PSP; n = 31), were inclu
210 rely in Idiopathic Parkinson's Disease(IPD), Progressive Supranuclear Palsy(PSP) or Multiple System A
211 ed blink rate, and vergence dysfunction, and progressive supranuclear palsy-related lid retraction, f
212 tween the corticobasal degeneration- and the progressive supranuclear palsy-related metabolic topogra
213 expression values for a previously validated progressive supranuclear palsy-related pattern provided
214 living patients with Alzheimer's disease and progressive supranuclear palsy relative to controls [mai
216 Nineteen patients with clinically diagnosed progressive supranuclear palsy (Richardson's syndrome),
217 e cerebellar variant of MSA (MSA-C), 17 with progressive supranuclear palsy-Richardson syndrome (PSP-
219 ssive aphasia (the corticobasal degeneration/progressive supranuclear palsy set), anterior temporal l
220 ain (t = 2.1, P < 0.04); while patients with progressive supranuclear palsy showed, relative to contr
221 nt mutation (R5L) was identified in a single progressive supranuclear palsy subject that was not in t
222 lear palsy subject that was not in the other progressive supranuclear palsy subjects or in 96 control
225 tion, associated with Pick, corticobasal and progressive supranuclear palsy subtypes of tau pathology
226 emporal dementia with FUS pathology; and the progressive supranuclear palsy syndrome with progressive
227 der the term frontotemporal dementia and the progressive supranuclear palsy syndrome, corticobasal sy
229 and higher availability of binding sites on progressive supranuclear palsy tau deposits for 11C-PBB3
231 ment in script size' are also more common in progressive supranuclear palsy than in Parkinson's disea
232 egeneration from multiple system atrophy and progressive supranuclear palsy (the two most common atyp
235 mer's disease, corticobasal degeneration and progressive supranuclear palsy using the Interpersonal R
241 ssive apraxia, corticobasal degeneration and progressive supranuclear palsy were, with one exception,
242 pokinesia without decrement in patients with progressive supranuclear palsy, which differed from the
243 evaluating the clinicopathologic markers of progressive supranuclear palsy, which have helped establ
244 11 with multiple system atrophy, and 13 with progressive supranuclear palsy) who were followed up for
245 sed in the SN in multiple system atrophy and progressive supranuclear palsy with an identical localis
246 red with patients with pathologically proven progressive supranuclear palsy with Richardson syndrome
247 l pathology in corticobasal degeneration and progressive supranuclear palsy without labeling the pred
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