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

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

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

5 eveal pathophysiological differences between parkinsonian and essential tremor circuits.

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

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

8 In parkinsonian animals, motor deficits were causally attri

9 d S2 terminals in VApc and CM of control and parkinsonian animals.

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

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

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

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

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

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

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

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

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

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

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

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

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

23 response to L-DOPA in the dopamine-depleted parkinsonian brain.

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

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

26 we used D5R knockout mice that were rendered parkinsonian by unilateral 6-OHDA injection.

27 g by visualising the dopamine transporter in parkinsonian cases.

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

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

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

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

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

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

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

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

36 Both normal movements and parkinsonian deficits in this task have striking homolog

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

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

39 lations that show different vulnerability to parkinsonian degeneration.

40 nd might prime subpopulations of neurons for parkinsonian degeneration.

41 might prime subpopulations of DA neurons for parkinsonian degeneration.

42 Parkinsonian diseases comprise a heterogeneous group of

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

44 We report a novel gene for a parkinsonian disorder.

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

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

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

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

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

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

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

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

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

54 verall brain functional activity for various parkinsonian disorders.

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

56 pporting a link between PLA2G6 mutations and parkinsonian disorders.

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

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

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

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

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

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

63 The anti-parkinsonian effects of tropicamide were almost complete

64 lockade by scopolamine produces similar anti-parkinsonian effects.

65 nt model of the complex movement deficits of Parkinsonian fallers, here we first demonstrated that ma

66 cholinergic-dopaminergic losses observed in Parkinsonian fallers.

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

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

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

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

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

72 en seen after TBI, but patients usually lack parkinsonian features.

73 d with neurodegeneration, cognitive loss and parkinsonian features.

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

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

76 signs in Parkinson's disease (PD), including parkinsonian gait, are often asymmetric, but mechanisms

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

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

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

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

81 rAAV-GFP injected LID-resistant hemi-parkinsonian Lewis rats displayed mild LID and no induct

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

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

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

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

86 xpressing cells, into the striatum initiated Parkinsonian-like pathological features in mice.

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

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

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

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

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

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

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

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

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

96 o levodopa, and were on stable doses of anti-parkinsonian medication were eligible.

97 rs of motor symptoms, and stable use of anti-parkinsonian medications for 28 days before consent.

98 lesome dyskinesias, with no increase in anti-parkinsonian medications.

99 These data argue that in parkinsonian mice abnormal, temporally offset prototypic

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

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

102 tegies alleviated motor-learning deficits in parkinsonian mice, pointing to a potential new therapeut

103 These studies revealed that in parkinsonian mice, the functional connectivity of PFn ne

104 ty in totally denervated striatal regions in parkinsonian mice.

105 mediate motor function and drug responses in parkinsonian mice.

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

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

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

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

110 the prevalence of "As" terminals in VApc of parkinsonian monkeys was 51.4% lower than in controls.

111 luT1-positive boutons in both VApc and CM of parkinsonian monkeys was significantly larger than in co

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

113 pc and CM did not differ between control and parkinsonian monkeys.

114 ocircuits in the VApc and CM of MPTP-treated parkinsonian monkeys.

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

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

117 ally intact cohort, a cohort with unilateral Parkinsonian motor deficits due to midbrain lesioning, a

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

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

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

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

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

123 6-Hydroxydopamine lesion led to parkinsonian motor impairment that was partially reverse

124 vation of basal ganglia circuitry underlying parkinsonian motor impairments.

125 covariate effects of cognitive capacity and parkinsonian motor impairments.

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

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

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

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

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

131 The results suggest that parkinsonian motor signs are absent in these patients wi

132 Parkinsonian motor signs are common in the aging populat

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

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

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

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

137 internus (GPi) is an effective treatment for parkinsonian motor signs.

138 the first to predict clinical improvement of parkinsonian motor symptoms across cohorts based on loca

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

140 te optogenetic STN DBS can indeed ameliorate parkinsonian motor symptoms through reduction of abnorma

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

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

143 plantation has shown promise in ameliorating parkinsonian motor symptoms.

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

145 interneurons alleviates motor symptoms in a parkinsonian mouse model.

146 s to investigate the neural underpinnings of parkinsonian movement deficits in the motor cortex of ch

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

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

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

150 n diseases ranging from malaria infection to Parkinsonian neurodegeneration.

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

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

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

154 ) to record neuronal population responses in parkinsonian nonhuman primates during subthalamic nucleu

155 ng high-density microelectrode arrays in two parkinsonian nonhuman primates each implanted with DBS l

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

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

158 submentalis and anterior tibialis muscles in parkinsonian patients (53 synucleinopathy, 24 tauopathy)

159 Here, activity was recorded from 10 awake, parkinsonian patients (6 male, 4 female human subjects)

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

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

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

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

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

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

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

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

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

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

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

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

172 pigmented neurons in the substantia nigra of parkinsonian patients.

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

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

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 1 display reduced mitophagy in the brain and parkinsonian phenotypes, including loss of tyrosine hydr

184 ssible through TracMouse and revealed subtle Parkinsonian phenotypes.

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

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

190 Acute parkinsonian rats executed <20 reaches, displaying marke

191 ild-type (WT) rats in a similar manner as in Parkinsonian rats lacking endogenous PTEN-induced kinase

192 hat expression of Nurr1 in l-DOPA naive hemi-parkinsonian rats resulted in the formation of morpholog

193 ings in multiple basal ganglia structures of parkinsonian rats revealed that these dynamics were reca

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

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

196 lation is critical for improving reaching in parkinsonian rats.

197 rons (MSNs) in drug-naive rAAV-injected male parkinsonian rats.

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

199 amatically ameliorated locomotor deficits in parkinsonian rats.

200 ation and accelerated functional recovery in Parkinsonian rats.

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

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 vioral effects were documented in normal and parkinsonian rodents.

209 cells were transplanted into male or female 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 nt sleep behaviour disorder (iRBD) exempt of Parkinsonian signs compared to healthy control subjects.

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

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

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

216 ple system atrophy patients with predominant parkinsonian signs had a higher number of red flag featu

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

218 3.56; 95% CI, 1.52-8.28) and progression of parkinsonian signs in ROS and MAP (odds ratio [OR] for T

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

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

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

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

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

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

225 aling with pathophysiological aspects of the parkinsonian state.

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

227 rgoes significant synaptic remodeling in 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 d rAAV2/5 to overexpress Nurr1 or GFP in the parkinsonian striatum of LID-resistant Lewis or LID-pron

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

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

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

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

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

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

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

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

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 egeneration into consideration when modeling parkinsonian symptoms.

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

245 ither necessary nor sufficient for relief of parkinsonian symptoms.

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

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

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

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

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

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

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

253 paminergic lesion associated with an evident parkinsonian syndrome.

254 degree of clinical overlap between atypical parkinsonian syndromes (APS) and Parkinson's disease (PD

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

274 egenerative conditions, such as dementia and parkinsonian syndromes, both for research and for clinic

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

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

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

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

279 orticobasal degeneration from other atypical parkinsonian syndromes.

280 ogy or distinguish Parkinson's from atypical parkinsonian syndromes.

281 istinguish this disorder from other atypical parkinsonian syndromes.

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

283 longitudinal study of patients with atypical parkinsonian syndromes.

284 impact in patients with clinically uncertain 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 e functions, which has implications for anti-parkinsonian therapy.

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

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

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

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

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

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

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

295 30 years or older with possible or probable parkinsonian variant multiple system atrophy were random

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

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

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

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