ライフサイエンスコーパス: PSP

1 PSP Association, CBD Solutions, Medical Research Council

2 PSP clinical severity did not correlate with (18) F-flor

3 PSP differentiated between sepsis, infection and sterile

4 PSP had lower CSF N-terminal and C-terminal tau concentr

5 PSP induced the transcription factor Nrf2, which regulat

6 PSP is able to differentiate between septic and nonsepti

7 PSP modification via a bilaminar approach utilizing eith

8 PSP specimens showed higher iron burden in the cerebral

9 PSP was accurately predicted from the midbrain/brainstem

10 PSP/reg levels are elevated in cell culture and mouse mo

11 001); visuospatial subscore in PD (p=0.003), PSP (p=0.022) and CBD (p=0.0002); and MMSE in CBD (p=0.0

12 Autoradiography was performed in 1 PSP patient, with digital pathology used to quantify tau

13 s reaction, three fluorescent probes (PSP-1, PSP-2, and PSP-3) were synthesized and evaluated.

14 A total of 103 PSP patients were included.

15 s presenting findings on 6193 patients (1911 PSP, 4282 MSA) fulfilled the inclusion criteria.

16 riteria, from two separate cohorts: the 2011 PSP GWAS cohort, from brain banks based at the Mayo Clin

17 ain bank, which were obtained after the 2011 PSP GWAS, were used for a pooled analysis.

18 From 1999 to 2011, PSP was attempted in 91 patients with presumed noninvasi

19 type 2 studies) with 356 MSA-P patients, 204 PSP patients, 79 CBS patients, and 62 MSA-C patients wer

20 tients with clinical diagnoses of PD (n=31), PSP (n=33), CBS (n=14), MSA (n=31), AD (n=26) and FTD (n

21 n = 9), cerebellar type MSA (MSA-C, n = 7), PSP (n = 13), and PD (n = 30).

22 n = 9), cerebellar type MSA (MSA-C, n = 7), PSP (n = 13), and PD (n = 30).

23 This study defines a PSP-related intrinsic connectivity network in the health

24 testing of a screening strategy involving a PSP and its associated web-based Decision Support System

25 this study could result in the adoption of a PSP screening strategy across the EU; a step that would

26 e recapitulated the hallmark lesions of AGD, PSP and CBD.

27 In enzyme inhibitory assays, all PSP samples inhibited the enzymes alpha-amylase, alpha-g

28 (PSP, MSA) or cognitive symptoms (FTD, ALS, PSP) in the diseases.

29 Altogether, PSP-2 exhibits significant bioactivity at concentrations

30 three fluorescent probes (PSP-1, PSP-2, and PSP-3) were synthesized and evaluated.

31 a gender by diagnosis interaction in AD and PSP for most tau species, with lower concentrations for

32 AD and PSP were matched for severity using the clinical dementi

33 Dec 1, 2019, if individuals were alive), and PSP phenotype (with reference to the 2017 Movement Disor

34 Antibodies to SP1, CA6 and PSP occur in some patients with idiopathic dry eyes.

35 BD susceptibility loci and show that CBD and PSP share a genetic risk factor other than MAPT at 3p22

36 e previously demonstrated that human CBD and PSP tauopathy lysates (CBD-tau and PSP-tau) contain dist

37 taucipir uptake was able to separate CBD and PSP.

38 ch showed marked atrophy in AD, ALS, FTD and PSP (Crus I/II), and MSA and PSP (lobules I-IV), respect

39 he total phenotypic variance of AD, FTD, and PSP, respectively.

40 ants with clinical diagnosis of AD, FTD, and PSP.

41 D, ALS, FTD and PSP (Crus I/II), and MSA and PSP (lobules I-IV), respectively.

42 can data, the probabilities of IPD, MSA, and PSP were computed and used to classify each of the subje

43 trophy were found for AD, ALS, FTD, MSA, and PSP.

44 abolic covariance patterns for IPD, MSA, and PSP.

45 higher total tau and ptau levels than NC and PSP.

46 to SERT are significantly lower in MSA-P and PSP than in PD and MSA-C patients and might therefore be

47 to SERT are significantly lower in MSA-P and PSP than in PD and MSA-C patients and might therefore be

48 level differences were found between PD and PSP for MMSE and ACE-R (total score and subscores for at

49 erved that glucosylation of both rhamnan and PSP can increase resistance to bacteriophage predation a

50 biosynthesis scheme in which the rhamnan and PSP chains are independently synthesized from two distin

51 n CBD and PSP tauopathy lysates (CBD-tau and PSP-tau) contain distinct tau strains that propagate neu

52 strain potency between AD-tau, CBD-tau, and PSP-tau in non-Tg mice.

53 Finally, CBD-tau- and PSP-tau-injected mice showed spatiotemporal transmission

54 re disease than anti-SP1, anti-CA6, and anti-PSP.

55 ti-Ro, anti-La, anti-SP1, anti-CA6, and anti-PSP.

56 Neither anti-PSP nor anti-SP1 reached statistical significance becaus

57 o the pathophysiology of tauopathies such as PSP by promoting tau accumulation and neuronal cell deat

58 Because PSP is associated with tau protein abnormalities, there

59 ions and using discriminant analysis between PSP and PD, 100% sensitivity and 97% specificity was ach

60 tensor imaging (DTI) to distinguish between PSP and Lewy body disorders at the individual-subject le

61 erbal fluency subscore distinguished between PSP and PD with a high sensitivity (0.92) and specificit

62 rum autoantibodies against BPIFA1 and BPIFA2/PSP occurred in 30% and 67% of the APECED patients with

63 nd B-cells were not significantly changed by PSP.

64 ant (MSA-P), MSA cerebellar variant (MSA-C), PSP, CBS, and PD using combined quantitative data from a

65 Circulating PSP/reg levels are also increased in some patients with

66 Clinical PSP patients showed bilaterally elevated (18) F-flortauc

67 The FA score distinguished between clinical PSP and Lewy body disorders with an area under the curve

68 A patient with clinical PSP and pathological diagnosis of corticobasal degenerat

69 ld be searched for in patients with clinical PSP-like phenotypes and a behavioral variant of frontote

70 e affected network in patients with clinical PSP.

71 PSP affects immune populations, we compared PSP treatments both with and without prior incubation in

72 consecutive patients with autopsy-confirmed PSP from the Queen Square Brain Bank between January 201

73 upranuclear palsy/corticobasal degeneration (PSP/CBD) or multiple-system atrophy (MSA) by PET and cli

74 tions of brains derived from Pick's disease, PSP, and corticobasal degeneration patients who underwen

75 Globus pallidus binding best distinguished PSP patients from controls and PD (area under the curve

76 cellular antioxidant properties, especially PSP CF.

77 dentification of substrates of the essential PSP calcineurin (CN) has been exceptionally challenging

78 To what extent PSP modification is beneficial for peri-implant health h

79 erral center among 21 patients with familial PSP-like phenotypes.

80 ontrast enhancer and potential biomarker for PSP.

81 and MSA (HR=5.6) classified by PET, but for PSP/CBD only when diagnosed by clinical follow-up (HR=4.

82 ients meeting clinical research criteria for PSP (n = 33) to normal controls (n = 46) and patients me

83 n Parkinson Plus Syndrome study criteria for PSP.

84 okadaic acid (OA), and domoic acid (DA), for PSP, DSP, and ASP, respectively.

85 been identified as a strong risk factor for PSP.

86 ed mortality was significantly increased for PSP/CBD (HR=5.2) and MSA (HR=5.6) classified by PET, but

87 for MSA and 94% specificity and 94% PPV for PSP.

88 K2) are identified as novel drug targets for PSP and CBD.

89 electrophoresis fingerprinting technique for PSP identification and characterisation.

90 phalopathy, a successful tau therapeutic for PSP might inform treatment of other neurodegenerative di

91 odulation as a disease-modifying therapy for PSP and related tauopathies.

92 thology, davunetide could be a treatment for PSP.

93 Davunetide is not an effective treatment for PSP.

94 r Global Development, USAID, SHOPS (formerly PSP-One), The World Health Organization, DFID, Human Res

95 Two new downloads are available from PSP.

96 Commercially extracting pigments from PSP can be challenging due to firm texture and high poly

97 After concentration of the polyphenols from PSP, preparative separation into two fractions, designat

98 ntersect of missense mutations and PTMs from PSP, identifies over 25,000 PTMVars (PTMs Impacted by Va

99 Furthermore, PSP enhanced cellular glutathione concentrations and dec

100 Two patients had PSP-like phenotypes with dystonia, vertical gaze slownes

101 Pre-heating PSP significantly increased polyphenolic yields in a tem

102 To elucidate how PSP affects immune populations, we compared PSP treatmen

103 In PSP, apparent susceptibility was increased in the red nu

104 In PSP, PSP-Richardson's phenotype (univariate HR 2.53; 95%

105 ultivariate HR 1.22; 95% CI 0.83 to 1.80).In PSP and MSA, survival was predicted by early falls (mult

106 peutic targets to combat tau accumulation in PSP and CBD.

107 s of the pro-apoptotic protein appoptosin in PSP patients.

108 (dMT), a region that shows focal atrophy in PSP.

109 y endpoints were the change from baseline in PSP Rating Scale (PSPRS) and Schwab and England Activiti

110 significantly lower hypothalamic binding in PSP and MSA-P than PD.

111 Our study correlates bona fide changes in PSP and CBD brains with cellular models, identifies drug

112 athology and neuroinflammation colocalize in PSP, and that individual differences in subcortical tau

113 tau fragment concentrations are different in PSP compared with AD despite the presence of severe tau

114 : (18) F-flortaucipir uptake was elevated in PSP versus controls and PD patients in a pattern consist

115 osis of atypical parkinsonism, especially in PSP.

116 The most important areas of growth in PSP are in disease and isoform informatics.

117 of sepsis - signifying a steeper increase in PSP levels in septic patients as opposed to those exhibi

118 target of rapamycin (mTOR) were increased in PSP and CBD brains.

119 also suggested that the predominant iron in PSP is hemosiderin, not ferritin.

120 presynaptic DAT function is clearly lower in PSP patients than in PD and MSA-P patients and is clearl

121 the hypothalamus were significantly lower in PSP than in MSA-C patients, and we observed significantl

122 the hypothalamus were significantly lower in PSP than in MSA-C patients, and we observed significantl

123 nd putamen DAT function was clearly lower in PSP than in PD (caudate: 34.1% difference, g = -1.08, 95

124 sal degeneration had severe tau pathology in PSP-related brain structures with good correspondence be

125 or measuring clinical disease progression in PSP is the PSP Rating Scale score.

126 ct and track clinical disease progression in PSP.

127 The number of unique PTMs in PSP is now more than 450 000 from over 22 000 articles a

128 associated with increased ROCK1 and ROCK2 in PSP and CBD brains, whereas experiments in cellular and

129 owed a significant decrease of T2* signal in PSP compared with controls (-57%; P = .028).

130 strongly associated with shorter survival in PSP and MSA.

131 LRRK2 locus was associated with survival in PSP.

132 ted with disease progression and survival in PSP.

133 or effective disease-modifying treatments in PSP.

134 eneral type of surgical approach to increase PSP, either bilaminar or an apically positioned flap (AP

135 Analysis of biomarker kinetics (PSP, routine markers) was performed on 90 patients admit

136 that were structurally different from known PSP inhibitors, and few of these scaffolds were highly s

137 further identified as an endoribonuclease L-PSP (Liver-Perchloric acid-soluble protein) by shotgun m

138 (Germany), and the University College London PSP cohort, from brain banks and the PROSPECT study, a U

139 Postmortem tissue from age-matched PSP (n = 6) and control (n = 3) brains was imaged by usi

140 Moreover, PSP/reg expression is induced by the canonical chemical

141 with cerebellar areas implicated for motor (PSP, MSA) or cognitive symptoms (FTD, ALS, PSP) in the d

142 )I-FP-CIT SPECT binding to SERT between MSA, PSP, and PD.

143 " OR "SPET" and keywords related to PD, MSA, PSP, and CBS.

144 sonism to another diagnostic group (PD, MSA, PSP, or CBS) were included.

145 roup and identify differences between nfvPPA-PSP and nfvPPA-CBD both at presentation and longitudinal

146 [IQR] sentence comprehension correct: nfvPPA-PSP, 98% [80-100]; nfvPPA-CBD, 81% [65-98]; P = .08) wer

147 ificantly in age, sex, or handedness (nfvPPA-PSP group: median [interquartile range (IQR)] age, 74 [6

148 Depression Scale median [IQR] score: nfvPPA-PSP, 19 [3-28]; nfvPPA-CBD, 4 [0-16]; P = .04), and rela

149 peech Examination median [IQR] score: nfvPPA-PSP, 4 [2-7]; nfvPPA-CBD, 0 [0-4]; P = .02), depression

150 te matter atrophy were typical of the nfvPPA-PSP group, while greater gray matter atrophy and a trend

151 tuations in the AP waveform explain observed PSP variability.

152 the reductase and phosphatase activities of PSP-GPD multidomain enzymes may be modulated by post-tra

153 established the proliferative capability of PSP on various immune populations in peripheral blood mo

154 ut few pedigrees with familial clustering of PSP-like phenotypes have been described.

155 ; and a postmortem pathological diagnosis of PSP or CBD.

156 ents with a likely or confirmed diagnosis of PSP or MSA were eligible for inclusion.

157 The evidence regarding the effect of PSP modification via APF-based approaches on peri-implan

158 ic properties, the anti-angiogenic effect of PSP-2 might potentially translate also into anti-cancer

159 To test the anti-angiogenic effect of PSP-2, a recently developed high affinity Cu(I) chelator

160 Although the etiopathology of PSP is unknown, mutations in the MAPT/tau gene and expos

161 ed to be sensitive to pathologic features of PSP were identified (ie, the superior cerebellar peduncl

162 ncing of the DCTN1 gene in familial forms of PSP at a referral center among 21 patients with familial

163 CIT binding ratios in the caudate nucleus of PSP patients than in that of both PD and MSA-C patients.

164 CIT binding ratios in the caudate nucleus of PSP patients than in that of both PD and MSA-C patients.

165 Sixteen RCTs reported the outcomes of PSP modification therapy with bilaminar techniques, wher

166 s in substantia nigra and globus pallidus of PSP compared with control brains.

167 ant morphological changes in the presence of PSP-2, with thicker tubular walls and an overall decreas

168 iteria that recognise early presentations of PSP and operationalise diagnosis of the full spectrum of

169 s critical to the extraction and recovery of PSP anthocyanins, suitable for food use.

170 nvironmental toxins can increase the risk of PSP.

171 omized-controlled trials (RCTs) reporting on PSP outcomes was conducted to assess and compare differe

172 red to routine inflammatory biomarkers, only PSP demonstrated a significant interaction between time

173 observed between tau strains such that only PSP-tau and CBD-tau strains induce astroglial and oligod

174 The framework of OPUS-DOSP is based on OPUS-PSP, previously developed by us, with refinement and new

175 Overall PSP was achieved with a feasibility rate of 89% (n = 81)

176 ng ratios were significantly lower in MSA-P, PSP, and PD than MSA-C patients.

177 Progressive supranuclear palsy (PSP) and corticobasal degeneration (CBD) are neurodegene

178 Studies of progressive supranuclear palsy (PSP) and corticobasal degeneration (CBD) suggest that mi

179 diagnosis of progressive supranuclear palsy (PSP) and Lewy body disorders, which include Parkinson di

180 se (PD) from progressive supranuclear palsy (PSP) and multiple system atrophy (MSA), which have simil

181 atients with progressive supranuclear palsy (PSP) and multiple system atrophy (MSA).

182 les from two progressive supranuclear palsy (PSP) cases and a MAPT P301L mutation carrier.

183 CBD with top progressive supranuclear palsy (PSP) GWAS single-nucleotide polymorphisms (SNPs) identif

184 Progressive supranuclear palsy (PSP) has been conceptualized as a large-scale network di

185 ggregates in progressive supranuclear palsy (PSP) have yielded mixed results.

186 Progressive supranuclear palsy (PSP) is a movement disorder characterized by tau neuropa

187 Progressive supranuclear palsy (PSP) is a neurodegenerative disorder characterized by th

188 Progressive supranuclear palsy (PSP) is a rare and progressive neurodegenerative conditi

189 Because progressive supranuclear palsy (PSP) is linked to tau pathology, davunetide could be a t

190 Progressive supranuclear palsy (PSP) is usually sporadic, but few pedigrees with familia

191 (nfvPPA) and progressive supranuclear palsy (PSP) or corticobasal degeneration (CBD) proved by autops

192 atients with progressive supranuclear palsy (PSP) Richardson's syndrome.

193 cal-dominant progressive supranuclear palsy (PSP) tau topologies.

194 hy (MSA) and progressive supranuclear palsy (PSP) than in Parkinson disease (PD), we hypothesized tha

195 PD), 30 with progressive supranuclear palsy (PSP), 19 with corticobasal degeneration (CBD).

196 thology, and progressive supranuclear palsy (PSP), a primary tauopathy characterised by deposition of

197 rophy (MSA), progressive supranuclear palsy (PSP), and corticobasal syndrome (CBS) have signs and sym

198 PSs) such as progressive supranuclear palsy (PSP), multiple system atrophy (MSA) and corticobasal syn

199 Progressive supranuclear palsy (PSP), multiple system atrophy (MSA) and idiopathic Parki

200 Progressive supranuclear palsy (PSP), previously believed to be a common cause of atypic

201 on (CBD) and progressive supranuclear palsy (PSP), tau also aggregates in astrocytes and oligodendroc

202 hy (MSA) and progressive supranuclear palsy (PSP), the most common atypical parkinsonian look-alike s

203 survival in progressive supranuclear palsy (PSP).

204 ase (AD) and progressive supranuclear palsy (PSP).

205 a (FTD), and progressive supranuclear palsy (PSP).

206 cific versus progressive supranuclear palsy (PSP).

207 ic factor in progressive supranuclear palsy (PSP).

208 AD (AD-tau), progressive supranuclear palsy (PSP-tau), and corticobasal degeneration (CBD-tau) patien

209 n = 32), and progressive supranuclear palsy (PSP; n = 31), were included in our cohort for diagnostic

210 d with FTLD (progressive supranuclear palsy [PSP], n = 10; corticobasal degeneration [CBD], n = 10; F

211 In selected patients, PSP for presumed noninvasive IPMN in experienced hands i

212 rial surface, named polysaccharide pellicle (PSP), and a more conserved rhamnan chain anchored to, an

213 ponents rhamnan and polysaccharide pellicle (PSP), respectively, whereas csdEF plays a role in galact

214 The peri-implant soft tissue phenotype (PSP) encompasses the keratinized mucosa width (KMW), muc

215 e with a putative phosphoserine phosphatase (PSP) motif fused to glycerol-3-phosphate dehydrogenase (

216 Phosphoserine phosphatase (PSP), a key essential metabolic enzyme involved in conve

217 our phosphine sulfide-stabilized phosphine (PSP) ligand design strategy, crisp-17 offers a Cu(I) dis

218 tection systems, such as pre-spotted plates (PSP), reduce analysis time while increasing capacity.

219 Paralytic shellfish poisoning (PSP) is a serious human illness caused by the ingestion

220 e presence of paralytic shellfish poisoning (PSP), diarrheic shellfish poisoning (DSP), and amnesic s

221 Polysaccharopeptide (PSP), from Coriolus versicolor, has been used as an adju

222 -PSP injections (13.7%) to 1483 of 5253 post-PSP injections (28.2%), a change of 14.6% (95% CI, 13.0%

223 -PSP injections (61.3%) to 1503 of 5253 post-PSP injections (28.6%), a change of -32.7% (95% CI, -34.

224 -PSP injections (25.0%) to 1838 of 5253 post-PSP injections (35.0%), a change of 10.0% (95% CI, 8.2%

225 Administration approval) to 429 of 5253 post-PSP injections (8.2%), a change of 8.2% (95% CI, 7.4% to

226 he deep purple color of purple sweet potato (PSP) is due to the high content of acylated anthocyanins

227 Purple sweet potatoes (PSP) have been used as a natural food colorant with high

228 This study described a potential PSP scenario in the Mediterranean Sea.

229 Post-synaptic potential (PSP) variability is typically attributed to mechanisms i

230 pt injections increased from 614 of 4488 pre-PSP injections (13.7%) to 1483 of 5253 post-PSP injectio

231 b injections increased from 1122 of 4488 pre-PSP injections (25.0%) to 1838 of 5253 post-PSP injectio

232 acizumab use decreased from 2752 of 4488 pre-PSP injections (61.3%) to 1503 of 5253 post-PSP injectio

233 Predominant PSP anthocyanins included acylated cyanidin or peonidin

234 Among the probes prepared, PSP-3 showed a desirable off/on fluorescence response to

235 on this reaction, three fluorescent probes (PSP-1, PSP-2, and PSP-3) were synthesized and evaluated.

236 ncreatic stone protein/regenerating protein (PSP/reg) is a potential biomarker for ER stressed beta c

237 member 2 (BPIFA2)/parotid salivary protein (PSP), and lactoperoxidase, 3 salivary-enriched proteins.

238 6 (CA6) and anti-parotid secretory protein (PSP), which occur early in the course of SS.

239 drase 6 (CA6) and parotid secretory protein (PSP).

240 the usefulness of pancreatic stone protein (PSP) as a powerful diagnostic and prognostic marker in c

241 In PSP, PSP-Richardson's phenotype (univariate HR 2.53; 95% CI 1

242 PhosphoSitePlus((R)) (PSP), a knowledgebase dedicated to mammalian post-transl

243 Our results therefore reveal PSP/reg as a potential biomarker for beta cells under ch

244 f the three cell wall glycopolymers rhamnan, PSP, and LTA, thus indicating that its function is share

245 Rhp-PSP exhibited significant inhibitory activities against

246 Herein, this protein is designated Rhp-PSP.

247 The screening PSP was developed to detect all GMOs authorized in the E

248 d across FTLD pathologies and could separate PSP and CBD.

249 ensitivity and 90% specificity in separating PSP from MSA.

250 The Movement Disorders Society PSP diagnostic criteria include syndromes with few or mi

251 region in France with a cluster of sporadic PSP cases.

252 In the present study, PSP-derived polyphenols were identified using HPLC-PDA a

253 sive supranuclear palsy-Richardson syndrome (PSP-RS), and 10 healthy subjects were recruited.

254 It was found that PSP significantly increased the number of monocytes (CD1

255 aortic ring assay and CAM assay showed that PSP-2 evokes significantly longer sprouts with smaller a

256 Overall, these results suggest that PSP extracts exhibit enzyme inhibitory and cellular anti

257 The PSP-LV can be a site of origin of VAs, which can be succ

258 The PSP-LV is anatomically adjacent to the inferior and medi

259 Difference in drug use before and after the PSP requirement for bevacizumab and the physicians' reas

260 Neuropathological examination confirmed the PSP diagnosis in the first two subjects; the MAPT P301L

261 ntricular arrhythmias (VAs) arising from the PSP-LV and describe a mapping and ablation approach from

262 g clinical disease progression in PSP is the PSP Rating Scale score.

263 gmentation procedures aimed at modifying the PSP and their impact on peri-implant health.

264 aling cellular antioxidant properties of the PSP extracts were investigated in cultured cells.

265 calisation signal for LRRK2, analysis of the PSP survival signal and eQTLs for LINC02555 in the eQTLG

266 ) axonal noise alone can explain half of the PSP variability in cerebellar synapses.

267 Mapping of the PSP-LV from the adjacent inferomedial RA was performed a

268 Mapping and ablation of the PSP-LV with an RA approach under intracardiac echocardio

269 From the RA side of the PSP-LV, a small atrial signal and a larger ventricular s

270 t the patients' clinical severity (using the PSP rating scale).

271 sitivity of network-based imaging methods to PSP-related physiological and clinical changes.

272 Event-related analysis demonstrated tripled PSP serum levels within 72 hours and doubled levels with

273 olved in l-serine biosynthesis including two PSP homologs: Rv0505c (SerB1) and Rv3042c (SerB2).

274 may be useful for differentiating underlying PSP from CBD pathology during life.

275 ecificity of the new criteria for underlying PSP pathology.

276 d symptoms that are suggestive of underlying PSP pathology and could provide an opportunity for earli

277 riteria also include definitions for variant PSP syndromes with different patterns of movement, langu

278 rior-superior process of the left ventricle (PSP-LV) is the most inferior and posterior aspect of the

279 We included 134 patients with PD, 11 with PSP, 10 with MSA and 44 healthy controls.

280 ease (224 with AD, 168 with FTD, and 48 with PSP) and in 224 control individuals without dementia enr

281 individuals of white European ancestry with PSP in stage one.

282 than have been conclusively associated with PSP pathology.

283 Compared with PSP, patients with CBS had atrophy connected to a networ

284 timulating monocyte/macrophage function with PSP could be an effective therapeutic intervention in ta

285 While incubation with PSP-2 resulted in selective depletion of cellular copper

286 n study (GWAS), we included individuals with PSP, diagnosed according to pathological and clinical cr

287 our finding suggests a genetic overlap with PSP.

288 In the validation cohort, 34 patients with PSP (69 years +/- 7; 22 women, 12 men), 25 patients with

289 ts In the discovery cohort, 16 patients with PSP (mean age +/- standard deviation, 73 years +/- 5; ei

290 ying treatment are feasible in patients with PSP and should be pursued with other promising tau-direc

291 al control (NC), 37 AD, and 24 patients with PSP participated in the study.

292 Furthermore, atrophy in patients with PSP progressed within the subcortical/brainstem motor sy

293 Patients with PSP showed significant connectivity disruptions within t

294 rmal connectivity pattern, and patients with PSP were compared to an independent matched healthy cont

295 To achieve this, 17 patients with PSP, 14 with IPD and 19 with MSA were scanned using stru

296 SA-P and those with MSA-C from patients with PSP-RS and those with PD.

297 Furthermore, patients with PSP-RS had significantly higher MD values in the vermis

298 and efficacy of davunetide in patients with PSP.

299 ession and reduced survival in patients with PSP.

300 h MSA-P from patients with PD and those with PSP-RS (P < .01; sensitivity, specificity, and positive