ライフサイエンスコーパス: DOPA

1 18F-DOPA imaging, however, suggested that intermittent conve

2 18F-DOPA PET imaging demonstrated a significantly increased

3 The influx constant kicer based on 18F-DOPA-PET was used to measure striatal dopamine synthesis

4 ous fluorodihydroxyphenyl-l-alanine PET (18F-DOPA-PET) and resting state functional MRI (rs-fMRI).

5 easen, and 24 healthy controls underwent 18F-DOPA-PET and behavioural-cognitive assessment.

6 rwent fluorodihydroxyphenyl-l-alanine ([18F]-DOPA) positron emission tomography to examine dopamine s

7 tched controls born at full term using [18F]-DOPA PET and structural MRI.

8 The incorporation of the amino acid DOPA (3,4-dihydroxyphenylalanine) allows the self-assemb

9 Herein, we study adhesion of Lys and DOPA-containing peptides to organic and inorganic substr

10 Both DOPA- and sugar-mediated bindings are reversible and rob

11 Furthermore, the covalent linkage induced by DOPA oxidation allows covalent capture of the aligned na

12 Disruption of bacterial signaling by DOPA modification reveals an infection containment strat

13 eurons, motor deficits that are improved byl-DOPA, and development of inclusion bodies.

14 c acid condenses with imino compounds (cyclo-DOPA or its glucosyl derivatives), or amines and/or thei

15 ation and its subsequent conversion to cyclo-DOPA, CYP76AD6 uniquely exhibits only tyrosine hydroxyla

16 ncluding Naproxen, (S)-Flurbiprofen, and a d-DOPA precursor.

17 ates the chiroselective oxidation of L- vs D-DOPA by H2O2.

18 ition or aryloxy radical coupling to form di-DOPA (3,4-dihydroxyphenylalanine).

19 urface-binding l-3,4-dihydroxyphenylalanine (DOPA) groups, pCB-(DOPA)4, were applied onto a paper-bas

20 ic role of (18)F-3,4-dihydroxyphenylalanine (DOPA) PET/CT at the time of staging in children with neu

21 , apfp-1) with L-3,4-dihydroxyphenylalanine (DOPA)-containing and mannose-binding domains has been ch

22 ine (Lys, K) and 3,4-Dihydroxyphenylalanine (DOPA, Y) residues in the mussel foot proteins (Mfps) has

23 istent with a stable dihydroxyphenylalanine (DOPA) radical.

24 es, we have identified at least two distinct DOPA-based cross-linking pathways during byssus fabricat

25 d substrate followed by 4-methylcatechol, DL-DOPA, and dopamine.

26 osttranslationally modified amino acid dopa (DOPA) in mussel adhesion, catechol functional groups hav

27 sion of dipeptides containing Lys and either DOPA (KY) or phenylalanine (KF) shows that DOPA is stron

28 In the kidney, the enzyme DOPA Decarboxylase (DDC) originating from the circulatio

29 inergic neurons, some of which still express DOPA decarboxylase (DDC).

30 rential effects between the 2 types of (18)F-DOPA in the 60-min accumulation experiment.

31 ross two independent cohorts underwent (18)F-DOPA PET scans to measure dopamine synthesis capacity (i

32 pocampal glutamate concentrations, and (18)F-DOPA PET was used to measure dopamine synthesis capacity

33 ng systems to (123)I-MIBG scanning and (18)F-DOPA PET/CT (i.e.,(123)I-MIBG WBS score and whole-body m

34 n chemotherapy, all patients underwent (18)F-DOPA PET/CT and (123)I-metaiodobenzylguanidine (MIBG) sc

35 o investigated the prognostic value of (18)F-DOPA PET/CT at the same time points.

36 ion-based analysis, the sensitivity of (18)F-DOPA PET/CT in detecting soft-tissue and bone or bone-ma

37 ion-based analysis, the sensitivity of (18)F-DOPA PET/CT in detecting soft-tissue and bone or bone-ma

38 Conclusion: (18)F-DOPA PET/CT is more sensitive than (123)I-MIBG WBS in st

39 (18)F-DOPA PET/CT results were compared with those of (123)I-M

40 94%, 92%, and 100%, respectively, for (18)F-DOPA PET/CT.

41 us 83%, 75% and 54%, respectively, for (18)F-DOPA PET/CT.

42 All received an (18)F-DOPA positron emission tomography (PET)/magnetic resonan

43 psychosis and 14 controls) received an (18)F-DOPA Positron Emission Tomography scan to measure DSC (K

44 (18)F-DOPA was produced via the novel synthesis method, yieldi

45 variate analysis, only posttherapeutic (18)F-DOPA WBMB (>7.5) was associated with progression-free su

46 ime-to-event analysis, posttherapeutic (18)F-DOPA WBMB remained the only risk factor associated with

47 -fluoro-3,4-dihydroxy-L-phenylalanine ((18)F-DOPA), involving the nucleophilic substitution of a diar

48 and dopamine synthesis capacity (using (18)F-DOPA, n = 21) within the ventral striatum.

49 At 37 degrees C, the uptake of both (18)F-DOPA-H and (18)F-DOPA-L did not differ significantly dur

50 (18)F-DOPA-H demonstrated comparable imaging properties in an

51 a the novel synthesis method, yielding (18)F-DOPA-H with a high specific activity (35,050 +/- 4,000 G

52 C, the uptake of both (18)F-DOPA-H and (18)F-DOPA-L did not differ significantly during a 60-min accu

53 several experiments with conventional (18)F-DOPA-L with a low specific activity (11 +/- 2 GBq/mmol).

54 al was 3 orders of magnitude less than (18)F-DOPA-L.

55 ns involved in the uptake mechanism of (18)F-DOPA.

56 iques (6-[fluoride-18]fluoro-levodopa [(18)F-DOPA] PET-CT and glucagon-like peptide 1 (GLP-1) recepto

57 e distribution volume ratio (EDVR) of [(18)F]DOPA influx rate to [(18)F]dopamine washout rate, an ind

58 ial topography observed here with the [(18)F]DOPA literature.

59 was assessed as K(i)(cer) value using [(18)F]DOPA PET before and 6 weeks after antipsychotic disconti

60 Furthermore, they also underwent an [(18)F]DOPA PET scan to quantify striatal dopamine synthesis ca

61 thesis capacity was measured by using [(18)F]DOPA PET.

62 To test this hypothesis, we performed [(18)F]DOPA positron emission tomography in 60 of the 87 partic

63 h striatal measures of dopamine using [(18)F]DOPA positron emission tomography, we show that higher p

64 matic state, we observed increases of [(18)F]DOPA uptake in the anterior putamen, [(11)C]raclopride b

65 CHR) for psychosis show elevations in [(18)F]DOPA uptake, an estimate of dopamine (DA) synthesis capa

66 dy the changes in dopamine synthesis ([(18)F]DOPA), dopamine D2/D3 receptors ([(11)C]raclopride), and

67 xy-6-[(18)F]-fluoro-l-phenylalanine ([(18)F]-DOPA) positron emission tomography (PET), we compared do

68 itself and other byssal proteins via Fe3(+)-DOPA complexes, and the mannose-binding domain interacts

69 We identified one dopamine synthesis gene, DOPA decarboxylase (DDC), as a suppressor of tau toxicit

70 presynaptic dopamine synthesis capacity (ie, DOPA decarboxylase activity).

71 pathogenic basiodiomycete forming an induced DOPA-melanin, Cryptococcus neoformans (CN); and the slow

72 es of l-carbidopa, which is known to inhibit DOPA decarboxylase (DDC), a key protein in Parkinson's d

73 l-DOPA also reverses the selective loss of dendritic "long

74 l-DOPA formation in red beet was found to be redundantly c

75 L-DOPA has been the gold standard for symptomatic treatmen

76 L-DOPA reinstatement of dopamine normalized HCN activity,

77 L-DOPA treatments could partially improve the movement imp

78 confirmed increased Nptx2 expression after L-DOPA and its blockade by SL327 using quantitative RT-PCR

79 TP, depotentiation, and LTP restored after L-DOPA treatment but also disclose multifaceted synaptic a

80 ed dopaminergic signaling is revived after l-DOPA treatment during early withdrawal.

81 zine, a 5-HT1A/B receptor agonist, against L-DOPA-induced dyskinesias in patients with Parkinson's di

82 l MOR1 levels and signaling and alleviates L-DOPA-induced dyskinetic movements in pituitary homeobox

83 ide therapeutic approaches for alleviating L-DOPA-induced dyskinesia in PD patients.

84 Mixtures of DA and L-DOPA at different molar rations were co-electropolymeriz

85 We found that prefrontal tDCS and l-DOPA both enhance neural activity in core regions of the

86 its role in experimental Parkinsonism and l-DOPA responses has been neglected.

87 n occurring under dopamine denervation and L-DOPA therapy.

88 od vessel formation when dexamethasone and l-DOPA were administered simultaneously.

89 tin via any chemical process (tyrosine and l-DOPA).

90 in dopamine release induced by l-DOPA and l-DOPA+dextroamphetamine.

91 ical parametric maps, indicating tDCS- and l-DOPA-induced activation, and >100 neuronal receptor gene

92 ation in rodent models of PD (PD mice) and L-DOPA-induced dyskinesia (LID mice).

93 such as Huntington's disease, dystonia and l-DOPA-induced dyskinesia in Parkinson's disease are all c

94 tested daily with L-DOPA to assess LID and L-DOPA-induced rotations.

95 sors and metabolites as norepinephrine and l-DOPA.

96 Because L-DOPA effects may be influenced by body weight, we repeat

97 1A and 5-HT1B receptors effectively blocks L-DOPA-induced dyskinesias in animal models of dopamine de

98 While CYP76AD1 catalyzes both l-DOPA formation and its subsequent conversion to cyclo-DO

99 se dopaminergic neuron loss and severe but L-DOPA-responsive motor defects in mouse overexpression mo

100 ate changes in dopamine release induced by l-DOPA and l-DOPA+dextroamphetamine.

101 nal program in striatal neurons induced by L-DOPA and triggered by the activation of ERK.

102 dentified a molecular signature induced by L-DOPA in the dopamine-denervated striatum that is depende

103 g) suppresses motor dysfunction induced by L-DOPA or D(2)R-selective agonists.

104 Restoration of dopamine transmission by l-DOPA relieves symptoms of PD but causes dyskinesia.

105 Restoration of dopamine transmission by l-DOPA relieves symptoms of PD but causes severe side effe

106 f motor control, which could be rescued by L-DOPA treatment.

107 synaptic dopamine availability induced by L-DOPA treatment.

108 KO mice was alleviated by donepezil and by l-DOPA, confirming an acetylcholine/dopamine deficit.

109 impairment that was partially reversed by l-DOPA.

110 s of dopamine, including GCH1 and TH cause l-DOPA-responsive dystonia.

111 ed uptake of a model substrate into cells (L-DOPA).

112 neurons become dysregulated during chronic L-DOPA administration and participate in the expression of

113 (6-OHDA) rendered dyskinetic with chronic L-DOPA treatment reveals a complex, Ras-GRF1 and pathway-i

114 ation of ChIs to dopamine loss and chronic L-DOPA treatment.

115 yskinesia-like effects of acute or chronic L-DOPA treatment.

116 e accumulation of FosB produced by chronic L-DOPA was reduced in MSK1 knockout.

117 ation of rapamycin with L-DOPA counteracts L-DOPA-induced dyskinesias in wild-type mice, but not in m

118 icient (DD) mice, which had received daily L-DOPA injections, could move effectively and even be hype

119 al neurons.SIGNIFICANCE STATEMENT To date, l-DOPA is the most effective treatment for PD.

120 ral delivery, can be avoided by delivering l-DOPA in a more continuous manner.

121 ntia nigra pars compacta and age-dependent L-DOPA-sensitive motor dysfunction.

122 unctioning by l-3,4-dihydroxyphenylalanin (l-DOPA) administration during early withdrawal.

123 ine (DA) and L-3,4-dihydroxyphenylalanine (L-DOPA) on carbon nano-onion (CNO) modified electrodes as

124 40 years ago l-3,4-dihydroxyphenylalanine (l-DOPA) therapy has retained its role as the leading stand

125 from chronic L-3,4-dihydroxyphenylalanine (L-DOPA) treatment, but the physiological basis of these ch

126 use model of L-3,4-dihydroxyphenylalanine (L-DOPA)-induced dyskinesia (LID) in Parkinson's disease (P

127 involved in L-3,4-dihydroxyphenylalanine (L-DOPA)-induced dyskinesia (LID) in Parkinson's disease sh

128 sease and in l-3,4-dihydroxyphenylalanine (l-DOPA)-induced dyskinesia (LID), a common motor complicat

129 sine to form l-3,4-dihydroxyphenylalanine (l-DOPA).

130 (DHPAA) from L-3,4-dihydroxyphenylalanine (L-DOPA).

131 By enhancing availability of dopamine, L-DOPA improved processing and gait speed in older adults

132 id and l-3,4-dihydroxyphenylalanine (i.e., l-DOPA), were attached to the shuttle.

133 epeated convergent acquisition of elevated l-DOPA 4,5-dioxygenase activity is consistent with recurre

134 se to polyphyletic occurrences of elevated l-DOPA 4,5-dioxygenase activity, accompanied by convergent

135 Glucose stimulation significantly enhances L-DOPA uptake, leading to increased DA release and GSIS re

136 and R1441C mutant transgenic rats exhibit L-DOPA-responsive motor dysfunction, impaired striatal dop

137 uced in the striatum of rodents expressing l-DOPA-induced dyskinesia (LID).

138 [(18)F]6-fluoro-L-DOPA ([(18)F]FDOPA) is a diagnostic radiopharmaceutical

139 We obtained baseline 6-[(18)F]fluoro-L-DOPA (FDOPA)-PET scans in 15 nonsmokers and 30 nicotine-

140 of genes aberrantly transcribed following l-DOPA treatment.

141 Following L-DOPA, global p11KO mice show reduced therapeutic respons

142 haracterised 23 distinct DODA proteins for l-DOPA 4,5-dioxygenase activity, from four betalain-pigmen

143 uently, improved our ability to screen for L-DOPA production.

144 Reference intervals for l-DOPA, catecholamines, and metanephrines in n = 115 healt

145 ichment of an enzyme-coupled biosensor for L-DOPA.

146 HP in a single enzyme system directly from L-DOPA both in vitro and in vivo, at higher yields than th

147 Very little is known about how L-DOPA therapy affects the dynamics of fluctuating dopamin

148 In support of our hypothesis, L-DOPA had no main effect on impulsive choice, but reduced

149 how it affects cholinergic interneurons in L-DOPA induced dyskinesia, we used D5R knockout mice that

150 over, we found that expression of Nurr1 in l-DOPA naive hemi-parkinsonian rats resulted in the format

151 We additionally determined that in l-DOPA-naive rats striatal rAAV-Nurr1 overexpression (1) i

152 catecholamine neurotransmitters, including L-DOPA, epinephrine, and norepinephrine.

153 cacy decreases, and side effects including l-DOPA-induced dyskinesia (LID) increase, affecting up to

154 escribe a three-round screen for increased L-DOPA production in S. cerevisiae using FACS enrichment o

155 ses total heme concentration and increases L-DOPA production, using dopamine measurement as a proxy.

156 atalyzes the conversion of l-tyrosine into l-DOPA, which is the rate-limiting step in the synthesis o

157 An acute dose of 5 mg/kg L-DOPA had no significant effect on dopamine dynamics, dem

158 In contrast, administration of 200 mg/kg L-DOPA significantly increased the amplitude of evoked dop

159 ins produced 0.91 g/L tyrosine or 0.41 g/L l-DOPA from 22.5 g/L unpurified SSW-derived chitin hydroly

160 nd even be hyperactive 72 h after the last L-DOPA injection when dopamine was almost completely deple

161 y boosting dopamine levels using levodopa (l-DOPA) as human subjects made economic decisions and repe

162 ia (LID) develops after repeated levodopa (l-DOPA) exposure in Parkinson disease patients and remains

163 ion that develops after repeated levodopa (l-DOPA) exposure in Parkinson disease patients.

164 study examined whether carbidopa/levodopa (L-DOPA) monotherapy increased dopamine availability, incre

165 e dose of the dopamine precursor levodopa (l-DOPA) on mesostriatal fractional amplitude of low-freque

166 uld occur on haloperidol than on levodopa (l-DOPA) or placebo.

167 tion of dopamine transmission by levodopa (L-DOPA) relieves motor symptoms of PD but often causes dis

168 and standard anti-Parkinson drug levodopa (l-DOPA).

169 nction and sometimes remedied by levodopa (L-DOPA).

170 in cultured neurons and causes a PD-like, l-DOPA-responsive motor phenotype in transgenic mice, was

171 We find that low l-DOPA 4,5-dioxygenase activity is distributed across the

172 of adeno-associated viral vector-mediated l-DOPA delivery to the putamen in 1-methyl-4-phenyl-1,2,3,

173 f-principle for continuous vector-mediated l-DOPA synthesis as a novel therapeutic strategy for Parki

174 n impulsive choice, we administered 150 mg L-DOPA to 87 healthy adults in a randomized, placebo-contr

175 In daDREAM mice, L-DOPA-induced dyskinesia was decreased throughout the ent

176 d that baseline impulsivity would moderate L-DOPA effects.

177 nefits of RA supplementation in moderating L-DOPA-induced dyskinesia.

178 Our findings suggest that D5R can modulate L-DOPA induced dyskinesia and is a critical activator of C

179 Moreover, L-DOPA therapy restored tNAA (9.1 +/- 0.4 vs 8.1 +/- 0.2;

180 combination with a suprathreshold dose of L-DOPA (Sinemet(R)) in 22 patients with Parkinson's diseas

181 The evolution of l-DOPA 4,5-dioxygenase activity, encoded by the gene DODA,

182 ylogeny, we then explored the evolution of l-DOPA 4,5-dioxygenase activity.

183 ctrode fouling caused by polymerization of L-DOPA and endogenous catecholamines on the electrode surf

184 an insects demonstrated that low levels of l-DOPA are rapidly metabolized into intermediates by pheno

185 iable tool that allows a better measure of L-DOPA augmented dopamine release in vivo, measured using

186 Microinjection of l-DOPA directly into the striatum ameliorated the dystonic

187 ovements but cerebellar microinjections of l-DOPA had no effect.

188 iSPNs abolished the therapeutic action of L-DOPA in PD mice.

189 This novel finding suggests the utility of l-DOPA in the field of implantable medical devices, such a

190 ation and participate in the expression of L-DOPA induced dyskinesia.

191 Our results show that the uptake of L-DOPA is essential for establishing intracellular DA stor

192 The constant, local supply of l-DOPA obtained with this approach holds promise as an eff

193 so exhibited baseline-dependent effects of L-DOPA on loss aversion and delay discounting.

194 inistration of caffeine with a low dose of l-DOPA reduces dyskinesia in animals with striatopallidal

195 circuits and represents a major target of L-DOPA therapy in Parkinson's disease.

196 kers for Parkinson disease and efficacy of L-DOPA therapy.

197 ic profile or antiparkinsonian efficacy of L-DOPA therapy.

198 e impact of CK2 ablation on the effects of l-DOPA treatment in the unilateral 6-OHDA lesioned mouse m

199 mical studies investigating the effects of L-DOPA treatment on electrically evoked dopamine release h

200 t to preliminarily evaluate the effects of L-DOPA treatment on the NM-MRI signal.

201 as enabled rapid and reliable detection of L-DOPA's effects on striatal dopamine signaling in intact

202 The use of l-DOPA, a small molecule drug shown to up-regulate VEGF in

203 Application of l-DOPA, on the other hand, increased blood vessel formatio

204 In the absence of L-DOPA, only chemogenetic stimulation of dSPNs mediated th

205 oncentration in the cerebrospinal fluid of L-DOPA-free PD patients.

206 iatonigral neurons reduces the severity of l-DOPA-induced dyskinesia (LID), a finding that correlates

207 herapy is complicated by the appearance of L-DOPA-induced dyskinesia (LID).

208 oprazine caused a significant reduction of L-DOPA-induced dyskinesias on area under the curves of Cli

209 ining neurons underlies the development of L-DOPA-induced dyskinesias.

210 mine may participate in the development of L-DOPA-induced dyskinesias.

211 ts, we generated a knock-in mouse model of l-DOPA-responsive dystonia (DRD) mice that recapitulates t

212 of Nurr1 expression in striatal neurons of l-DOPA-treated PD patients.

213 expression can be found in the putamen of l-DOPA-treated PD patients.

214 patients (N = 15) who received 3 weeks of L-DOPA.

215 enervation and pulsatile administration of L-DOPA.

216 tal Nurr1 despite receiving a high dose of l-DOPA.

217 ng frequency significantly increased in ON L-DOPA dyskinetic 6-hydroxydopamine-lesioned rats, suggest

218 The impact of DREAM on L-DOPA efficacy was evaluated using the rotarod and the cy

219 fected offspring suffered from early-onset l-DOPA-responsive Parkinson's disease.

220 itron emission tomography followed by open L-DOPA for 3 weeks (1 week each of 150 mg, 300 mg, and 450

221 th time, however, the shortcomings of oral l-DOPA treatment have become apparent, particularly the mo

222 Therefore, targeting beta-arrestins in PD L-DOPA therapy might prove to be a desirable approach.

223 tained with the optimal dose of peripheral l-DOPA.

224 plicated in 3,4-dihydroxy-l-phenylalanine (L-DOPA)-induced dyskinesia (LID), a motor complication aff

225 amine function (dihydroxy-L-phenylalanine; L-DOPA) reduces the impact of valence on information-seeki

226 ed glassy carbon electrodes to form a poly(L-DOPA/DA) film.

227 imating equations tested the pre- and post-L-DOPA differences in processing and gait speed measures,

228 gic signaling using the dopamine precursor l-DOPA (l-3,4-dihydroxyphenylalanine) or dopamine receptor

229 we assessed the roles of the DA precursor L-DOPA in beta-cell DA synthesis and release in conjunctio

230 e by examining the effect of its precursor L-DOPA on the choices of healthy human participants in an

231 , administration of the dopamine precursor l-DOPA reversed the presynaptic deficit by restoring the b

232 assessed the ability of NM-MRI to predict L-DOPA treatment response in a subset of these patients (N

233 In parkinsonian rats, l-DOPA administration reduced M1 glutamate efflux and enha

234 Among sham-lesioned rats, l-DOPA did not change glutamate or GABA efflux.

235 nd treatment whereby, among lesioned rats, l-DOPA given acutely (1 d) or chronically (14-16 d) reduce

236 Parkinson's disease patients will receive l-DOPA and eventually develop hyperkinetic involuntary mov

237 ion of delay more strongly after receiving L-DOPA, whereas the opposite was detected for those with l

238 ansmission could contribute to the reduced L-DOPA responsivity.

239 uronal cells and the PD-relevant stressor, L-DOPA.

240 Subchronic L-DOPA increases levels of adaptor protein p11 (S100A10) i

241 Subchronic l-DOPA treatment of TAAR1 KO mice unilaterally lesioned wi

242 Supplying l-DOPA during withdrawal re-establishes synaptic morpholog

243 c slices reveal that both in vivo systemic l-DOPA administration and in vitro exposure to dopamine ca

244 were assessed for LID following long-term L-DOPA administration.

245 evelopment of involuntary movements termed l-DOPA-induced dyskinesia.

246 We previously proposed that l-DOPA 4,5-dioxygenase activity evolved via a single Caryo

247 We find that L-DOPA causes parkin loss through both oxidative stress-in

248 We previously reported that L-DOPA effects on reward-based decision-making in a random

249 Together, these findings demonstrate that l-DOPA induces widespread changes to striatal DNA methylat

250 erall, the present study demonstrates that l-DOPA-induced dyskinesia is associated with increased M1

251 microinjections into M1 demonstrated that l-DOPA-induced dyskinesia was reduced by M1 infusion of a

252 Local gene delivery of the l-DOPA synthesizing enzymes, tyrosine hydroxylase and guan

253 sened locomotor performance in response to L-DOPA and enhanced LID scores.

254 it is a genetic modifier of sensitivity to l-DOPA and of nicotine neuroprotection in PD.

255 The enhanced behavioral sensitization to l-DOPA in TAAR1 KO mice was paralleled by increased phosph

256 tor of cholinergic activity in response to L-DOPA in the dopamine-depleted parkinsonian brain.

257 y major roles in the cellular responses to l-DOPA in the striatum, these findings prompted us to exam

258 eased LHb neuronal activity in response to L-DOPA is related to AIM manifestation.

259 taining neurons have a reduced response to L-DOPA on the therapeutic parameters, but develop dyskinet

260 tNAA and tCr levels are responsive to L-DOPA therapy.

261 e striatopallidal knock-out in response to l-DOPA treatment.Our work shows, in a rodent model of PD,

262 dSPNs exacerbated dyskinetic responses to L-DOPA, while stimulation of iSPNs inhibited these respons

263 mptoms of Parkinson's Disease (PD), and to L-DOPA-induced dyskinesia.

264 a progressive motor disorder responsive to l-DOPA.

265 talyzes the hydroxylation of L-tyrosine to L-DOPA.

266 bit tremor and rotational responses toward L-DOPA, but develop less dyskinesia.

267 ies with chronic oral eltoprazine to treat l-DOPA-induced-dyskinesias.

268 imultaneous quantification of unconjugated l-DOPA, catecholamines, and metanephrines in plasma by LC-

269 n about potential gains than losses, under L-DOPA this difference was not observed.

270 ce, which was absent in control mice under l-DOPA treatment only.

271 udying the molecular mechanisms underlying L-DOPA therapy and also promises to benefit a wide variety

272 Using l-DOPA as a model substrate, biochemical assays in large L

273 a more refined dopaminergic therapy where l-DOPA is delivered continuously at the site where it is n

274 e and D-serine in the monkey putamen while L-DOPA rescues both D-amino acids levels.

275 ocessing and gait speed were observed with L-DOPA (450-mg dose: processing speed factor score effect

276 term treatment of Parkinson's disease with l-DOPA almost always leads to the development of involunta

277 NM-MRI signal 3 weeks post-treatment with L-DOPA compared to baseline (200 of 1807 SN-VTA voxels; P(

278 reover, coadministration of rapamycin with L-DOPA counteracts L-DOPA-induced dyskinesias in wild-type

279 te of ChIs, whereas chronic treatment with L-DOPA of lesioned mice increases baseline ChI firing rate

280 ding to dyskinesia in animals treated with L-DOPA or D1 receptor agonists.

281 rr1 agonist amodiaquine (AQ) together with l-DOPA or ropinirole.

282 nistration, animals were tested daily with L-DOPA to assess LID and L-DOPA-induced rotations.

283 gly, repeated M2 stimulation combined with l-DOPA treatment produced an unanticipated improvement in

284 their sustantia nigra or by treatment with l-DOPA, suggesting that alpha-SYN regulates dopamine avail

285 e/six female; 66.6 +/- 8.8 years old) with L-DOPA-induced dyskinesias.

286 ts known as dyskinesia upon treatment with L-DOPA.

287 In this work, l-DOPA was used for the first time as a pro-angiogenic age

288 h 1 mg/g of the DDC inhibitor L-alpha-Methyl-DOPA and 0.75 mg/g of the TH inhibitor 3-iodo-tyrosine (

289 This work shows the combination of DOPA and sugar chemistry at asymmetric interfaces is unp

290 loading studies revealed that the density of DOPA on the surface of the nanoscale MOF correlates to t

291 Here, we investigated the various fates of DOPA residues in proteins comprising mussel byssus fiber

292 ver, the complex topological relationship of DOPA and Lys as well as the interfacial adhesive roles o

293 rotonin, and trace amines, relies in part on DOPA decarboxylase (DDC, AADC), an enzyme that is requir

294 ion converts p-Tyr to protein-bound dopa (PB-DOPA) via a tyrosinyl radical intermediate, thereby alte

295 4-dihydroxyphenylalanine (DOPA) groups, pCB-(DOPA)4, were applied onto a paper-based sensor surface v

296 The capability of pCB-(DOPA)4-modified paper sensor for specific antigen-antibo

297 s) with 1,2-dioleoyl-sn-glycero-3-phosphate (DOPA) is presented.

298 300 nM 1,2-dioleoyl-sn-glycero-3-phosphate (DOPA), but not the control 1,2-dioleoyl-sn-glycero-3-pho

299 r DOPA (KY) or phenylalanine (KF) shows that DOPA is stronger and more versatile.

300 een the byssus and soft tissue, that is, the DOPA-containing domain interacts with itself and other b