ライフサイエンスコーパス: PSP

1 PSP binds PtdIns(3,4)P(2), 10-fold greater than PtdIns(3

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

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

4 PSP induced the transcription factor Nrf2, which regulat

5 PSP specimens showed higher iron burden in the cerebral

6 PSP was accurately predicted from the midbrain/brainstem

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

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

9 Sixty-nine (62.7%) of the 110 PSP cases were classified as RS and 29 (26.4%) as PSP-P.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

25 rated that a subset of patients with CBD and PSP present with a progressive apraxia of speech, nonflu

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

27 Corticobasal degeneration and PSP are neurodegenerative diseases characterized by neur

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

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

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

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

32 mal structure occur in the SN in PD, MSA and PSP and that these are similar in nature suggesting that

33 tive cells in the SN of control, PD, MSA and PSP brain.

34 a6 subunits TH-positive cells in PD, MSA and PSP compared to control tissue.

35 More than 50% of the MSA and PSP patients died over the year.

36 oms in patients with late stage IPD, MSA and PSP.

37 roteasomal subunits in the SN in PD, MSA and PSP.

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

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

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

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

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

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

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

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

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

47 h PSP into 'Richardson's syndrome' (RS) and 'PSP-parkinsonism' (PSP-P).

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

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

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

51 ases were classified as RS and 29 (26.4%) as PSP-P.

52 Because PSP is associated with tau protein abnormalities, there

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

54 experimental and clinical trials that blood PSP levels rise in the presence of inflammation or infec

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

56 A single viral RNA labeled by PSP can be directly observed in MDCK cells.

57 Furthermore, saccades produced by PSP patients had equivalent properties whether they were

58 strongly associated with a diagnosis of CBD, PSP, or both.

59 e then show that, in our sample of IC cells, PSP directional selectivity is not created de novo.

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

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

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

63 e affected network in patients with clinical PSP.

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

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

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

67 eye movement feature that best distinguished PSP patients from controls.

68 cellular antioxidant properties, especially PSP CF.

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

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

71 ontrast enhancer and potential biomarker for PSP.

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

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

74 n Parkinson Plus Syndrome study criteria for PSP.

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

76 omplexes very desirable luminescent dyes for PSP.

77 been identified as a strong risk factor for PSP.

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

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

80 imal thoracoscopic pleurodesis procedure for PSP with high recurrence risk remains controversial.

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

82 electrophoresis fingerprinting technique for PSP identification and characterisation.

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

84 thology, davunetide could be a treatment for PSP.

85 Davunetide is not an effective treatment for PSP.

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

87 Two new downloads are available from PSP.

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

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

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

91 Furthermore, PSP enhanced cellular glutathione concentrations and dec

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

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

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

95 Human PSP synthesized in vitro also binds PtdIns(3,4)P(2).

96 In PSP an RS phenotype, male gender, older age of onset and

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

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

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

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

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

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

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

104 by the same neural circuit and that, both in PSP patients and in controls, SWJs result from a couplin

105 on of PA700-Rpt5 subunits was not changed in PSP or PD but was significantly increased in MSA compare

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

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

108 pairment (P = 0.03) also occurred earlier in PSP than in MSA.

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

110 ent, larger, and more markedly horizontal in PSP patients than in healthy human subjects.

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

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

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

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

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

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

117 ct and track clinical disease progression in PSP.

118 ational saccades (microsaccades) are rare in PSP.

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

120 erebellum impairment, fixational saccades in PSP are abnormally large and thus more likely to trigger

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

122 strongly associated with shorter survival in PSP and MSA.

123 We moreover determined that, in PSP patients and controls, the larger the saccade the mo

124 Clinical variants in PSP reflect varying anatomical distribution of tau patho

125 is for anatomical selective vulnerability in PSP and its variants remains to be determined.

126 LSP approach is inferior to the integrating PSP approach.

127 y luminescent divalent osmium complexes into PSP.

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

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

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

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

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

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

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

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

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

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

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

139 tuations in the AP waveform explain observed PSP variability.

140 he study concerns the diagnostic accuracy of PSP in predicting acute appendicitis and therefore the e

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

142 Binding of PSP to PtdInsPs may contribute to sorting during the for

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

144 history of pathologically confirmed cases of PSP and MSA.

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

146 T) in a patient with a clinical diagnosis of PSP and assessed its frequency in multiple independent s

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

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

149 lyses of clinical and pathologic features of PSP indicate that there are distinct clinicopathologic v

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

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

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

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

154 of clinical and pathologic presentations of PSP and its variants.

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

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

157 T locus is associated with increased risk of PSP and Parkinson's disease.

158 -center, cohort study to assess the value of PSP in the diagnostic workup of acute appendicitis.

159 -center, cohort study to assess the value of PSP in the diagnostic workup of acute appendicitis.

160 In variants of PSP presenting with focal cortical syndromes, such as fr

161 In variants of PSP presenting with levodopa-responsive Parkinsonism, as

162 e are distinct clinicopathologic variants of PSP.

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

164 As OPUS-PSP excludes interactions among main-chain atoms, its su

165 Moreover, OPUS-PSP does not explicitly include solvation terms, and thu

166 derived from side-chain packing, named OPUS-PSP.

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

168 Overall, OPUS-PSP is a generally applicable potential for protein stru

169 Although the OPUS-PSP block-based orientation-dependent, side-chain atom c

170 ing patients with a diagnosis of IPD, MSA or PSP, stages 3-5 Hoehn and Yahr(H&Y).

171 d no immunoreactivity was detected in MSA or PSP.

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

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

174 Pressure sensitive paints (PSP) that measure the changes in air pressure have prove

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

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

177 cluding FTD, progressive supranuclear palsy (PSP) and corticobasal syndrome, and a common extended ha

178 defined for progressive supranuclear palsy (PSP) and multiple system atrophy (MSA).

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

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

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

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

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

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

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

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

187 es, of which progressive supranuclear palsy (PSP) is one of the most common, are clinically heterogen

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

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

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

191 hy (MSA) and progressive supranuclear palsy (PSP) where nigral dopaminergic neurones also degenerate.

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

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

194 me (CBS) and progressive supranuclear palsy (PSP), both of which have prominent eye movement abnormal

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

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

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

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

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

200 s, including progressive supranuclear palsy (PSP).

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

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

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

204 Disease(IPD), Progressive Supranuclear Palsy(PSP) or Multiple System Atrophy(MSA).

205 son's syndrome' (RS) and 'PSP-parkinsonism' (PSP-P).

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

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

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

209 event and (2) propagating surface plasmons (PSP) which integrate a great number of simultaneously oc

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

211 synthesis of the paralytic shellfish poison (PSP), (+)-gonyautoxin 3, is described.

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

213 detection of paralytic shellfish poisoning (PSP) toxins in shellfish as an alternative to the increa

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

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

216 ercentage of tumor nuclei staining positive (PSP) was quantified manually or by image analysis, and t

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

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

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

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

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

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

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

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

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

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

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

228 Predominant PSP anthocyanins included acylated cyanidin or peonidin

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

230 tide probe, call a polymeric sequence probe (PSP), was used to detect influenza A (Influenza A/WSN/33

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

232 ble cargo protein Parotid Secretory Protein (PSP) is bound to the membranes of secretory granules iso

233 6 (CA6) and anti-parotid secretory protein (PSP), which occur early in the course of SS.

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

235 Pancreatic Stone Protein (PSP) is a protein naturally produced mainly in the pancr

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

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

238 Bacterially expressed rat PSP binds PtdIns(3,4)P(2) with a K(d) of 2.4 x 10(-11) M

239 Rhp-PSP exhibited significant inhibitory activities against

240 Herein, this protein is designated Rhp-PSP.

241 RNA-PSP identified the following unique trends: 5'UNNNC3' lo

242 Interestingly, the results from RNA-PSP are able to qualitatively predict specificity based

243 sing the RNA Privileged Space Predictor (RNA-PSP) program show that each aminoglycoside preferentiall

244 eveloped RNA Privileged Space Predictor (RNA-PSP) program, which analyzes selected sequences to ident

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

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

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

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

249 rm that RS had a less favourable course than PSP-P, and that early autonomic failure in MSA is associ

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

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

252 The PSP Appendix Trial is a prospective, multi-center, cohor

253 The PSP is a single-stranded DNA molecule with ~2,000 tandem

254 The PSP-1 RNA binding domain is required for its colocalizat

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

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

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

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

259 METHODS/DESIGN: The PSP Appendix Trial is a prospective, multi-center, cohor

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

261 pathways were differentially affected in the PSP group, with a significant alteration of pontothalami

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

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

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

265 ponse of the LSP-based sensor to that of the PSP-based sensor.

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

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

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

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

270 either technique is appropriate for treating PSP patients with high recurrence risk.

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

272 s greater cortical pathology than in typical PSP.

273 cleus and substantia nigra - than in typical PSP.

274 iochemical and genetic features with typical PSP.

275 ferences, not temporal differences, underlie PSP directionality.

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

277 ecificity of the new criteria for underlying PSP pathology.

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

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

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

281 However, it is not known whether PSP is superior to other established blood tests (e.g. W

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

283 than have been conclusively associated with PSP pathology.

284 of early symptoms, we subdivided cases with PSP into 'Richardson's syndrome' (RS) and 'PSP-parkinson

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

286 Ten patients with PSP and 12 healthy volunteers underwent dynamic [123I]-i

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

288 Patients with PSP had an older age of onset (P < 0.001), but similar d

289 red with control participants, patients with PSP had binding potential values that were unchanged in

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

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

292 Patients with PSP reached their first clinical milestone earlier than

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 rom disease onset, compared to patients with PSP-P.

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

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

299 and efficacy of davunetide in patients with PSP.

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