ライフサイエンスコーパス: parkinsonian

1 1) amphetamine-induced rotations in the hemi-Parkinsonian 6-hydroxydopamine (6-OHDA)-treated rat and

2 mine neurons restores motor function in hemi-parkinsonian, 6-hydroxy-dopamine-lesioned rats.

3 inhibition in the STN, which contributes to parkinsonian activity and motor dysfunction.

4 e considered as novel disease-modifying anti-Parkinsonian agents, which are much needed for the thera

5 h-to-grasp task in either acute drug-induced parkinsonian akinesia (0.03-0.07 mg/kg haloperidol, s.c.

6 eveal pathophysiological differences between parkinsonian and essential tremor circuits.

7 opographies generated in multiple cohorts of parkinsonian and healthy macaques.

8 opyridine (MPTP) intoxication to render them parkinsonian and then local stereotaxic lesion of the PP

9 In parkinsonian animals, motor deficits were causally attri

10 Importantly, in parkinsonian animals, two main types of GP neuron were i

11 iring rate and pattern have been reported in parkinsonian animals.

12 indicative of increased synaptic activity in parkinsonian animals.

13 one sufficiently and instantaneously induced parkinsonian-associated locomotor dysfunction in normal

14 o the striatum of C57Bl/6 mice to model hemi-Parkinsonian attributes.

15 xerts a normalizing effect on the downstream parkinsonian basal ganglia firing patterns.

16 ile beta oscillations often occur within the parkinsonian basal ganglia, how these oscillations emerg

17 The first model assumes that Parkinsonian beta oscillation are generated in the corte

18 etting activity in the STN-GP network during Parkinsonian beta oscillations, suggesting they arise fr

19 type-selective entrainment of SPN firing to parkinsonian beta oscillations.

20 escribe the mechanisms for generation of the Parkinsonian beta oscillations.

21 For example, there is evidence that parkinsonian bradykinesia and rigidity may arise from an

22 ndrial dysfunction in parkin mutants induces Parkinsonian bradykinesia via a neuronal energy deficit

23 Depleted of dopamine, the dynamics of the parkinsonian brain impact on both 'action' and 'resting'

24 lecule drug shown to up-regulate VEGF in the Parkinsonian brain, can potentially resolve these issues

25 of neuronal loss in the substantia nigra of parkinsonian brain.

26 e the elevated metabolic network activity in parkinsonian brains on an individual basis.

27 adrenergic neuronal loss in monkeys rendered parkinsonian by chronic treatment with low doses of 1-me

28 g by visualising the dopamine transporter in parkinsonian cases.

29 f beta oscillations, which are a hallmark of parkinsonian circuit dysfunction.

30 ehaviour disorder but lower than in the hemi-parkinsonian cohort.

31 n the patients with this disorder and in the parkinsonian cohorts but decreased with disease progress

32 The knowledge obtained recently on atypical parkinsonian conditions points out the major deficits in

33 ders, have started being studied on atypical parkinsonian conditions, and although preliminary result

34 expanding phenotypical spectrum of atypical parkinsonian conditions, the early identification of pat

35 rtico-BG-thalamo-cortical loop in normal and parkinsonian conditions.

36 We observed StartReact in healthy and Parkinsonian controls.

37 that Cu(II)(atsm) is effective in reversing parkinsonian defects in animal models and has the potent

38 restore striatal dopamine levels and improve parkinsonian deficits, but the mechanisms underlying the

39 Nigral iron elevation is also a feature of Parkinsonian degeneration that may be related to soluble

40 might prime subpopulations of DA neurons for parkinsonian degeneration.

41 lations that show different vulnerability to parkinsonian degeneration.

42 nd might prime subpopulations of neurons for parkinsonian degeneration.

43 de insights into early metabolic features of parkinsonian dementia.

44 Parkinsonian disability was associated with robust and w

45 corded continuously throughout conditions of parkinsonian disability, its reversal, and the exhibitio

46 Parkinsonian diseases comprise a heterogeneous group of

47 deficiency syndrome is the first identified parkinsonian disorder caused by genetic alterations of t

48 ients with spontaneous RBD will convert to a parkinsonian disorder within a decade.

49 We report a novel gene for a parkinsonian disorder.

50 etic alteration in DAT function underlying a parkinsonian disorder.

51 done poorly), investigate pathophysiology of parkinsonian disorders (yes, if done carefully), play a

52 s high specificity in distinguishing between parkinsonian disorders and could help in selecting treat

53 Sixteen patients with parkinsonian disorders had a dual examination with (18)F

54 Clearly delineating parkinsonian disorders into subclasses on the basis of m

55 Here, we test the hypothesis that other parkinsonian disorders such as multiple system atrophy a

56 redict diagnosis in individual patients with Parkinsonian disorders, and identifies distinct patterns

57 se (PD) diagnosis, differential diagnosis of Parkinsonian disorders, and monitoring disease progressi

58 be helpful in the differential diagnosis of parkinsonian disorders, and thereby facilitate the devel

59 In idiopathic Parkinson disease and atypical parkinsonian disorders, central dopaminergic and overall

60 is an urgent need for biomarkers to diagnose parkinsonian disorders, particularly in the early stages

61 For cognition in parkinsonian disorders, this notion developed into the c

62 stural instability are disabling features of Parkinsonian disorders, treatable with pedunculopontine

63 imer disease, dementia with Lewy bodies, and parkinsonian disorders.

64 are linked to typical Parkinson's disease or parkinsonian disorders.

65 verall brain functional activity for various parkinsonian disorders.

66 (18)F-FDG PET for differential diagnosis of parkinsonian disorders.

67 pporting a link between PLA2G6 mutations and parkinsonian disorders.

68 approximately 18 months to 135 patients with parkinsonian disorders: 86 with idiopathic Parkinson's d

69 Experimentally induced and parkinsonian disruptions in dopamine (DA) transmission a

70 The best-characterized Parkinsonian DJ-1 missense mutation, L166P, disrupts hom

71 date examining clinical response to an anti-parkinsonian drug and the first to be conducted in patie

72 are major targets of antipsychotic and anti-Parkinsonian drugs, a better characterization of Drd3 si

73 dopaminergically insensitive aspects of the parkinsonian dysexecutive syndrome, yet the direct effec

74 ner receptors can be applied in the study of Parkinsonian dysfunction to understand the mechanisms be

75 The anti-parkinsonian effects of tropicamide were almost complete

76 lockade by scopolamine produces similar anti-parkinsonian effects.

77 006, patients from the New York area who had parkinsonian features but uncertain clinical diagnosis h

78 plicated in PD and many animal models induce parkinsonian features by disrupting mitochondrial functi

79 ion of HtrA2 was previously shown to lead to parkinsonian features in motor neuron degeneration (mnd2

80 inent nigral degeneration and the associated parkinsonian features of Parkinson's disease.

81 ogeneous Mecp2 expression contributes to the parkinsonian features of RTT in Mecp2(+/-) mice.

82 ile), laryngeal dystonia and, in some cases, parkinsonian features, and do not respond to levodopa th

83 time when medication effect has worn off and parkinsonian features, including bradykinesia and rigidi

84 d with neurodegeneration, cognitive loss and parkinsonian features.

85 trophysiological methods in monkeys rendered parkinsonian following chronic exposure to low doses of

86 s of pedunculopontine nucleus stimulation on Parkinsonian gait disturbance are not established.

87 There was good discriminatory power between parkinsonian groups, dementia disorders and healthy cont

88 eas the status of striatal discharges in the parkinsonian human brain remains conjectural.

89 ly reflect the degree of objective change in parkinsonian impairment or disability.

90 ur in subclasses of SPNs upon induction of a parkinsonian lesion followed by chronic levodopa treatme

91 he role of ChI activity in the expression of parkinsonian-like motor deficits in a unilateral nigrost

92 Finally, SChI activation led to parkinsonian-like motor deficits in otherwise normal mic

93 ial targets for the symptomatic treatment of parkinsonian-like motor symptoms.

94 r resulting in elevated manganese levels and parkinsonian-like movement deficits.

95 y lead to the development of an irreversible parkinsonian-like syndrome that has no treatment.

96 ation of early pathophysiological, and later parkinsonian-like, alterations.

97 ges may by itself serve as a direct cause of parkinsonian locomotor deficits, even in the absence of

98 charges in the subthalamic nucleus (STN) and parkinsonian locomotor symptoms.

99 uclear palsy (PSP), the most common atypical parkinsonian look-alike syndromes (APS), can be clinical

100 g retinal pigment epithelial (hRPE) cells in parkinsonian macaques and evaluated the reproducibility

101 e, two subjects with Gaucher disease without parkinsonian manifestations showed diminished striatal d

102 Moreover, anti-parkinsonian medication restored the ability to maximize

103 Patients were on their anti-Parkinsonian medication throughout the study.

104 were collected while patients were Off anti-parkinsonian medications under three stimulation conditi

105 However, in parkinsonian mice we found that cortico-STN transmission

106 gic tone attenuates the expression of LID in parkinsonian mice with established dyskinesia after chro

107 Derivation of 187 ntES cell lines from 24 parkinsonian mice, dopaminergic differentiation, and tra

108 ty in totally denervated striatal regions in parkinsonian mice.

109 mediate motor function and drug responses in parkinsonian mice.

110 We evaluated STN DBS in a parkinsonian model that displays alpha-synuclein patholo

111 The present study attempted to model GIDs in parkinsonian monkeys and, for the first time, to test th

112 f the cortico-basal ganglia-thalamic loop in parkinsonian monkeys revealed abnormal highly synchroniz

113 r territory) was 26.1% lower in MPTP-treated parkinsonian monkeys than in controls.

114 pa treatment in improving sleep disorders in parkinsonian monkeys, and that adding a cholinergic PPN

115 Using extracellular recordings in severely parkinsonian monkeys, we examined the activity changes o

116 rtico-subthalamic projection in MPTP-treated parkinsonian monkeys.

117 lity is demonstrated by transplantation into parkinsonian monkeys.

118 ulation of the cortico-subthalamic system in parkinsonian monkeys.

119 cortico-subthalamic transmission ameliorates parkinsonian motor deficits without eliciting any vivid

120 mice that had recovered from lesion-induced Parkinsonian motor deficits, light-induced selective sil

121 ays a central role in the pathophysiology of parkinsonian motor deficits.

122 ective therapeutic strategy for ameliorating parkinsonian motor deficits.

123 Major secondary outcomes included parkinsonian motor disability, activities of daily livin

124 eatment value) in daily "on" time (relief of parkinsonian motor features) without troublesome dyskine

125 6-Hydroxydopamine lesion led to parkinsonian motor impairment that was partially reverse

126 covariate effects of cognitive capacity and parkinsonian motor impairments.

127 vation of basal ganglia circuitry underlying parkinsonian motor impairments.

128 level-dependent fluctuations in the resting Parkinsonian motor network-disclosing the distributed ef

129 , striatal dopamine, nigral cell counts, and parkinsonian motor ratings in the same animals.

130 -treated monkeys had significantly improved parkinsonian motor ratings, greater striatal FD and DTBZ

131 tonomic dysfunction, cognitive function, and parkinsonian motor signs (using the Unified Parkinson's

132 role for several loci in the development of parkinsonian motor signs and nigral pathology in older p

133 Parkinsonian motor signs are common in the aging populat

134 ovement-related activity in M1 contribute to parkinsonian motor signs but are not consistent with the

135 vity in one frequency spectrum or the other, parkinsonian motor signs may relate more to the developm

136 e a central factor in the pathophysiology of parkinsonian motor signs.

137 ilar time course as that of the reduction in parkinsonian motor signs.

138 cle, were performed until the development of parkinsonian motor symptoms in either of the two experim

139 s correlated well with the induction of hemi-parkinsonian motor symptoms.

140 plantation has shown promise in ameliorating parkinsonian motor symptoms.

141 ork that are closely related to movement and parkinsonian motor symptoms.

142 cating the thalamus as playing a key role in Parkinsonian motor symptoms.

143 -disrupted animals show neuroprotection in a parkinsonian mouse model.

144 mes of basal ganglia organization posit that parkinsonian movement difficulties presenting after stri

145 Parkinsonian movement disorders are often associated wit

146 tion (HFS) is clinically recognized to treat parkinsonian movement disorders, but its mechanisms rema

147 Parkinson's disease (PD) has emphasized that parkinsonian movement, although bradykinetic, shares man

148 n diseases ranging from malaria infection to Parkinsonian neurodegeneration.

149 d NO production in astrocytes exposed to the parkinsonian neurotoxicant 1-methyl-4-phenyl-1,2,3,6-tet

150 tched with expression changes induced by the Parkinsonian neurotoxin rotenone and opposed by those in

151 LID without enhancing striatal DA release in parkinsonian non-human primates.

152 l-1,2,3,6-tetrahydropyridine (MPTP)-rendered Parkinsonian nonhuman primate model of l-DOPA-induced dy

153 ng-lasting aftereffects on motor function in parkinsonian nonhuman primates.

154 at the loss of Parkin did not exacerbate the parkinsonian pathology already present in the mice, but

155 ients (age 62.6+/-5.0 years) and 16 moderate parkinsonian patients (age 56.9+/-12.2 years).

156 pattern and examine its evolution in 21 hemi-parkinsonian patients (age 62.6+/-5.0 years) and 16 mode

157 ty has been reported in the basal ganglia of parkinsonian patients and animal models of the disease.

158 entials from the pedunculopontine nucleus in parkinsonian patients during rest and unconstrained walk

159 Neural activity in the brain of parkinsonian patients is characterized by the intermitte

160 During unconstrained walking, Parkinsonian patients who experience gait freezing had r

161 ls, to compare in vivo glutamate function in parkinsonian patients with and without levodopa-induced

162 w target for deep brain stimulation (DBS) in parkinsonian patients with gait disturbance and postural

163 However, StartReact was absent in Parkinsonian patients with severe gait freezing and post

164 perimental conditions, while OFF medication, Parkinsonian patients with severe gait freezing implante

165 Results were compared to Parkinsonian patients without gait freezing matched for

166 mine transporter imaging was abnormal in all parkinsonian patients, indicating Parkinson's disease-li

167 a target for deep brain stimulation (DBS) in parkinsonian patients, particularly for symptoms such as

168 nded evidence that in a specific subgroup of Parkinsonian patients, stimulation of a caudal pedunculo

169 y, by recording LFP activity from the STN in parkinsonian patients, we demonstrate that perimovement

170 ective long term follow-up study of incident parkinsonian patients.

171 ndency to resonate at approximately 20 Hz in Parkinsonian patients.

172 pigmented neurons in the substantia nigra of parkinsonian patients.

173 erminals, as well as in peripheral organs of Parkinsonian patients.

174 l burden in the CNS at birth and developed a parkinsonian phenotype after exposure to chronic systemi

175 eted striata of MitoPark mice that express a parkinsonian phenotype because of severe respiratory cha

176 ramming and maintenance of DNs, results in a parkinsonian phenotype featuring progressive degeneratio

177 tening, mediated in part by autophagy, and a parkinsonian phenotype in transgenic mice; however, the

178 use DA neurons leads to a slowly progressing parkinsonian phenotype in which motor impairment is firs

179 cause of Kufor-Rakeb syndrome (KRS), a rare parkinsonian phenotype with juvenile onset.

180 ons could partly underlie the variability in parkinsonian phenotype.

181 GBA-associated parkinsonism exhibit varying parkinsonian phenotypes but tend to have an earlier age

182 ex I inhibitor with a known association with parkinsonian phenotypes in both human populations and ro

183 ssible through TracMouse and revealed subtle Parkinsonian phenotypes.

184 Here, we describe a French family with a parkinsonian-pyramidal syndrome harboring a novel hetero

185 s that might improve this therapy, we used a parkinsonian rat model to examine whether pregraft chron

186 e BG-thalamocortical network in the behaving parkinsonian rat.

187 s correlate with both nigral cell counts and parkinsonian ratings, we suggest that these SN PET measu

188 blockers to the subthalamic nucleus (STN) of parkinsonian rats and evaluated locomotor behaviors via

189 f control and 6-hydroxydopamine-treated hemi-parkinsonian rats anesthetized with isoflurane.

190 d Type-A GP (GP-TA) neurons in anaesthetised Parkinsonian rats during such oscillations to constrain

191 Acute parkinsonian rats executed <20 reaches, displaying marke

192 he effect of pregraft levodopa, one group of parkinsonian rats received levodopa for 4 weeks prior to

193 In parkinsonian rats, l-DOPA administration reduced M1 glut

194 We report here that, in parkinsonian rats, preexposure to chronic levodopa signi

195 bor in the external globus pallidus (GPe) of Parkinsonian rats, showing that the distinct temporal ac

196 splanted into the 6-hydroxydopamine lesioned Parkinsonian rats, these cografts of VM and Pitx3 overex

197 lation is critical for improving reaching in parkinsonian rats.

198 g rate and LTS-like events were abolished in parkinsonian rats.

199 amatically ameliorated locomotor deficits in parkinsonian rats.

200 prominent psychostimulantlike properties in Parkinsonian rats: (1) it produced intense reward on its

201 -induced rotations in severely-lesioned hemi-Parkinsonian rats; this effect was fully blocked by nalo

202 Parkinsonian rest and essential postural tremor severity

203 Such differences in parkinsonian rest and essential tremor will be important

204 Based on these results we conclude that parkinsonian rest tremor is driven by a neural network,

205 anges in tremor frequency that dictates that parkinsonian rest tremor may be significantly entrained

206 Specifically, the amplitude of parkinsonian rest tremor remained unchanged despite spon

207 Parkinsonian rodent models show enhanced reinforcing eff

208 f distinct circuit elements in freely moving parkinsonian rodents and found that therapeutic effects

209 vioral effects were documented in normal and parkinsonian rodents.

210 inetic macaques without affecting the global parkinsonian score.

211 Motor symptoms such as mild parkinsonian signs are common in older persons, but litt

212 isk estimates) were more likely to have mild parkinsonian signs compared with lower risk participants

213 pressing these three mutant variants.UPR and parkinsonian signs could be partially rescued by growing

214 UPR activation and development of parkinsonian signs could be recapitulated in flies expre

215 PD), potential genetic risk factors for mild parkinsonian signs have been largely unexplored.

216 3.56; 95% CI, 1.52-8.28) and progression of parkinsonian signs in ROS and MAP (odds ratio [OR] for T

217 mild cognitive impairment and progression of parkinsonian signs in ROS and MAP.

218 ning wild-type dopaminergic neurons improved parkinsonian signs to a similar extent as DATKO grafts,

219 nfolded Protein Response (UPR) and developed parkinsonian signs, manifested by death of dopaminergic

220 neuroleptic exposure, or 'soft age-related' parkinsonian signs.

221 Within each parkinsonian state (naive, mild, moderate, and severe),

222 After the induction of a parkinsonian state in mice, there was a progressive decl

223 citation of indirect-pathway MSNs elicited a parkinsonian state, distinguished by increased freezing,

224 In the parkinsonian state, dopamine influx produced both increa

225 he thalamus and explore the mechanism of the Parkinsonian state, the proposed method can be useful in

226 nd essential in the study of the thalamus in Parkinsonian state.

227 C may provide a noninvasive biomarker of the parkinsonian state.

228 vels observed in basal ganglia in normal and parkinsonian states.

229 es with high precision under both normal and Parkinsonian states.

230 ontribute to abnormal firing patterns in the parkinsonian STN.

231 olinergic drive, a condition relevant to the parkinsonian striatum, lead to enhanced beta oscillation

232 cal correlation, a condition relevant to the parkinsonian striatum.

233 milarly high (specificity and PPV > 90%) for parkinsonian subjects with short symptom duration.

234 maging to study an independent cohort of 129 parkinsonian subjects with uncertain diagnosis; 77 (60%)

235 ty commonly observed in the basal ganglia of parkinsonian subjects.

236 ecombinant human PDGF-BB (rhPDGF-BB) reduces Parkinsonian symptoms and increases dopamine transporter

237 ated with at least one use of drugs to treat parkinsonian symptoms and quetiapine with less akathisia

238 in terms of the magnitude of improvement in parkinsonian symptoms for those with the favourable resp

239 rostriatal function that precedes behavioral parkinsonian symptoms in this genetic PD model.

240 Overexposure to manganese (Mn) may lead to parkinsonian symptoms including motor deficits.

241 thus far unexplained clinical phenomena like parkinsonian symptoms that have sometimes been observed

242 efficacy of treatment, use of drugs to treat parkinsonian symptoms, weight gain, sedation, increase i

243 ropyridine/vehicle-treated animals displayed parkinsonian symptoms, whereas none of the 1-methyl-4-ph

244 egeneration into consideration when modeling parkinsonian symptoms.

245 e STN and that rescuing this loss alleviates Parkinsonian symptoms.

246 n should be monitored for the development of parkinsonian symptoms.

247 ced dyskinesia (LID) in an effort to improve parkinsonian symptoms.

248 nt to reduce neurochemical loss and decrease parkinsonian symptoms.

249 patients with clinically suspected atypical parkinsonian syndrome (APS) were prospectively recruited

250 lysosomal ATPase ATP13A2, a gene linked to a parkinsonian syndrome (Kufor-Rakeb syndrome), in brain s

251 On examination, he showed a severe parkinsonian syndrome featuring bradykinesia, rigidity (

252 supranuclear palsy is considered an atypical parkinsonian syndrome, it is not known whether patients

253 women presenting with a late-onset isolated parkinsonian syndrome.

254 ented with a 4-year history of a progressive parkinsonian syndrome.

255 paminergic lesion associated with an evident parkinsonian syndrome.

256 esirable in patients with suspected atypical parkinsonian syndromes (APSs) for optimal treatment and

257 This is important as atypical parkinsonian syndromes (APSs) such as progressive supran

258 rty-seven patients with clinically uncertain Parkinsonian syndromes (mean age +/- SD, 56.9 +/- 14.9 y

259 high diagnostic accuracy for differentiating parkinsonian syndromes (PS), from essential tremor and p

260 riatal dopaminergic pathways as seen in most parkinsonian syndromes and in some cases of illicit drug

261 nge of neurodegenerative diseases, including parkinsonian syndromes and motor neuron disease.

262 mination (ACE-R) could differentiate between parkinsonian syndromes and reflect longitudinal changes

263 atistical analyses for diagnosis of atypical parkinsonian syndromes are 91.4% and 90.6%, respectively

264 rogression were compared with other atypical Parkinsonian syndromes from previous QSBB studies.

265 1) were significantly lower in patients with parkinsonian syndromes in drug-off condition than in hea

266 with spectra obtained from 20 patients with parkinsonian syndromes in drug-on and drug-off condition

267 o compare healthy subjects and patients with parkinsonian syndromes in drug-on or drug-off conditions

268 contributor to the differential diagnosis of parkinsonian syndromes in the correct clinical context.

269 idiopathic Parkinson's disease from atypical parkinsonian syndromes is challenging, especially in the

270 Patients presenting with parkinsonian syndromes share many clinical features, whi

271 In comparison with other Parkinsonian syndromes the patients were older and had a

272 Fourteen patients with parkinsonian syndromes underwent (18)F-desmethoxyfallypr

273 metabolic diseases, and genetic dystonic or parkinsonian syndromes) and are, therefore, frequently m

274 anuclear palsy (the two most common atypical parkinsonian syndromes) on a single case basis.

275 in networks in Parkinson's disease, atypical parkinsonian syndromes, and other movement disorders.

276 between Parkinson disease (PD) and atypical parkinsonian syndromes, including multiple-system atroph

277 Patients with FoG, which is a feature of parkinsonian syndromes, show variability in gait metrics

278 In some patients with suspected parkinsonian syndromes, SPECT imaging with ((123)I)ioflu

279 When compared with other Parkinsonian syndromes, VP had an older age of onset.

280 impact in patients with clinically uncertain Parkinsonian syndromes.

281 orticobasal degeneration from other atypical parkinsonian syndromes.

282 istinguish this disorder from other atypical parkinsonian syndromes.

283 work-up of patients with known or suspected parkinsonian syndromes.

284 maging for diagnosing and managing different parkinsonian syndromes.

285 maging in patients with clinically uncertain Parkinsonian syndromes.

286 basal conditions, MSNs are more excitable in parkinsonian than in sham mice, and excitability decreas

287 inergic MN9D neuronal cells treated with the parkinsonian toxicant 1-methyl-4-phenylpyridinium (MPP(+

288 etwork approach to study the effects of anti-parkinsonian treatment on motor sequence learning in hum

289 Here, we demonstrate that parkinsonian tremors and ETs result from distinct patter

290 We included patients with parkinsonian type MSA (multiple-system atrophy with pred

291 Methods: We included patients with parkinsonian type MSA (multiple-system atrophy with pred

292 nese (Mn) toxicity causes an extrapyramidal, parkinsonian-type movement disorder with characteristic

293 Corticobasal degeneration is an uncommon parkinsonian variant condition that is diagnosed mainly

294 30 years or older with possible or probable parkinsonian variant multiple system atrophy were random

295 s with Parkinson disease (PD), nine with the parkinsonian variant of multiple system atrophy (MSA-P),

296 In this population of patients with the parkinsonian variant of multiple system atrophy, treatme

297 asagiline on symptoms and progression of the parkinsonian variant of multiple system atrophy.

298 presentation, but accurate distinction among Parkinsonian variants may be difficult; non-Parkinson's

299 riboflavin capsules), stratified by subtype (parkinsonian vs cerebellar), with a block size of four.

300 Toward this end, monkeys were rendered parkinsonian with n-methyl-4-phenyl-1,2,3,6-tetrahydropy