ライフサイエンスコーパス: DOPA

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

2 Z twin pairs underwent high-resolution [18F]-DOPA PET to assess presynaptic striatal dopamine functio

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

4 Using [18F]-DOPA positron emission tomography (PET), we sought to de

5 synthesis of protected forms of (R)-beta(3)-DOPA and L-DOPA from the same aziridine, the former by S

6 We used a DOPA-containing sequence motif as the starting point for

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

8 biochemical striatal dopamine depletion and DOPA-responsive dystonia, but also predisposes to nigros

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

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

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

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

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

14 0 gene that catalyzes the formation of cyclo-DOPA.

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

16 -polymer-modified quartz substrates toward D-DOPA, whereas no change was observed after treatment wit

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

21 ound that only l-3,4-dihydroxyphenylalanine (DOPA)-containing peptides were sufficient to maintain pa

22 ail to display l-3,4-dihydroxyphenylalanine (DOPA)-responsive parkinsonism and drug-resistant gait an

23 e recognition of 3,4-dihydroxyphenylalanine (DOPA).

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

25 or (18)F-FET were higher than those of (18)F-DOPA (4.0 +/- 2.0 and 4.9 +/- 2.3 vs. 3.5 +/- 1.6 and 4.

26 ignificantly higher for (18)F-FET than (18)F-DOPA (TBR SUV(mean): 3.8 +/- 1.7 vs. 3.4 +/- 1.2, P = 0.

27 son of high- and low-specific-activity (18)F-DOPA in a neuroendocrine tumor model to determine whethe

28 es in uptake pattern for (18)F-FET and (18)F-DOPA in patients with primary or recurrent HGG, both SUV

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

30 e progression, prospectively underwent (18)F-DOPA PET and conventional MR imaging, performed within 1

31 (18)F-DOPA PET data were interpreted qualitatively and semiqua

32 (18)F-DOPA PET was used to estimate dopamine synthesis capacit

33 (18)F-FET and (18)F-DOPA PET/CT images were compared visually and semiquanti

34 was to determine whether (18)F-FET and (18)F-DOPA PET/CT provide comparable information in HGG.

35 Thirty (18)F-FET and (18)F-DOPA PET/CT scans were obtained before surgery or biopsy

36 Our results indicate that (18)F-DOPA PET/MR image fusion may be a reliable imaging bioma

37 The contribution of (18)F-DOPA PET/MR image fusion was considered relevant if it e

38 nostic and therapeutic contribution of (18)F-DOPA PET/MR image fusion was relevant in 9 of 13 patient

39 (18)F-DOPA uptake by the basal ganglia was present (SUV(mean),

40 (18)F-DOPA uptake correlated significantly with progression-fr

41 The degree of (18)F-DOPA uptake in the basal ganglia (SUV(mean)) was also as

42 The (18)F-DOPA uptake pattern was heterogeneous in all positive sc

43 Significant differences in terms of (18)F-DOPA uptake were found between low- and high-grade lesio

44 tions between the degree and extent of (18)F-DOPA uptake, MR imaging tumor characteristics, and histo

45 's outcome was finally correlated with (18)F-DOPA uptake.

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

47 used (18)F-3,4-dihydroxyphenylalanine ((18)F-DOPA) PET/MR images in pediatric supratentorial IAs.

48 using (18)F-dihydroxyphenyl-L-alanine ((18)F-DOPA) positron emission tomography.

49 droxy-6-[(18)F]fluoro-L-phenylalanine ((18)F-DOPA) uptake in the striatum of subjects at ultra-high r

50 ydroxy-6-(18)F-fluoro-l-phenylalanine ((18)F-DOPA), and (11)C-methionine ((11)C-MET) detect primary a

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

52 e advantages of the novel synthesis of (18)F-DOPA, which relies on nucleophilic fluorination of a dia

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

54 nces in distribution and metabolism of (18)F-DOPA-H and (18)F-DOPA-L in carbidopa-pretreated mice.

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

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

57 emperature did not alter the uptake of (18)F-DOPA-H.

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

59 ion and metabolism of (18)F-DOPA-H and (18)F-DOPA-L in carbidopa-pretreated mice.

60 At 0 degrees C, the uptake of (18)F-DOPA-L was significantly decreased, whereas the lower te

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

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

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

64 gic behavior and imaging properties of (18)F-DOPA.

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

66 administered, pharmacologically active (19)F-DOPA.

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

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

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

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

71 xy-6-[(18)F]-fluoro-l-phenylalanine ([(18)F]-DOPA).

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

73 even in the absence of a family history for DOPA-responsive dystonia.

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

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

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

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

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

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

80 l-DOPA present in morinda additionally increases the size

81 l-DOPA-dependent deregulation of 28 genes was blocked by p

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

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

84 ility decreases toward normal values after L-DOPA treatment.

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

86 3,4-Dihydroxyphenyl-L-alanine (L-DOPA)-induced dyskinesia (LID) is a debilitating side ef

87 elopment of 3,4-dihydroxyphenyl-L-alanine (L-DOPA)-induced dyskinesia.

88 activate DREAM may be useful to alleviate L-DOPA-induced dyskinesia without interfering with the the

89 ons in Mutator mice degenerated causing an L-DOPA reversible motor deficit.

90 of protected forms of (R)-beta(3)-DOPA and L-DOPA from the same aziridine, the former by SmI2-mediate

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

92 ergic transmission, but its role in PD and l-DOPA responses has been neglected.

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

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

95 physiology in Parkinson's disease (PD) and L-DOPA-induced dyskinesia (LID).

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

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

98 sors and metabolites as norepinephrine and l-DOPA.

99 used in treating these disorders, such as L-DOPA for Parkinson's disease, methylphenidate for attent

100 nged use causes dyskinesias referred to as L-DOPA-induced dyskinesias (LIDs).

101 1A and 5-HT1B receptors effectively blocks L-DOPA-induced dyskinesias in animal models of dopamine de

102 vement in the dystonia in response to both l-DOPA and trihexyphenidyl.

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

104 Conversely, RO5166017 counteracted both l-DOPA-induced rotation and dyskinesia as well as AMPA rec

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

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

107 esicular content was markedly increased by L-DOPA or decreased by reserpine in a time-dependent manne

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

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

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

111 g a negative feedback on ERK activation by l-DOPA.

112 and indicate that this can be modulated by L-DOPA.

113 impairment that was partially reversed by l-DOPA.

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

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

116 s indicate that the combination of chronic L-DOPA and NET-mediated DA reuptake in lesioned nigrostria

117 Chronic L-DOPA induces abnormal spine re-growth exclusively in D2R

118 (6-OHDA) rendered dyskinetic with chronic L-DOPA treatment reveals a complex, Ras-GRF1 and pathway-i

119 Chronic L-DOPA treatment, which induced dyskinesia and aberrant Fo

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

121 with established dyskinesia after chronic L-DOPA treatment.

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

123 tion was similar between acute and chronic l-DOPA, SKF81297 caused the largest increase in striatal p

124 oating, poly(butadiene-maleic anhydride-co-L-DOPA) (PBMAD), to non-bioadhesive nanospheres resulted i

125 By contrast, L-DOPA failed to normalize fast-spiking interneuron activi

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

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

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

129 present a promising approach to decreasing L-DOPA-induced motor complications in Parkinson's disease.

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

131 A) precursor l-3,4-dihydroxyphenylalanine (L-DOPA), but its prolonged use causes dyskinesias referred

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

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

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

135 L-3,4-dihydroxyphenylalanine (L-DOPA)-induced dyskinesia is an incapacitating complicati

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

137 t with Levodopa [L-dihydroxyphenylalanine (L-DOPA)] is the gold standard treatment of Parkinson's dis

138 iated inhibition of DA uptake in the DMI + L-DOPA group compared with L-DOPA-alone group in lesioned

139 t groups, with increased ppERK1/2 in DMI + L-DOPA group compared with the L-DOPA- and DMI-alone group

140 dyskinetic effects in lesioned rats, DMI + L-DOPA-treated rats gradually expressed more severe dyskin

141 re abolished by the antiparkinsonian drug, L-DOPA, or by SKF81297, a dopamine D1-type receptor agonis

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

143 in vivo, caused by one injection of either l-DOPA or cocaine, induced adult-like, non-desensitizing D

144 Using an escalating L-DOPA dose protocol, LID severity was decreased in Narp k

145 Feeding with excess l-DOPA showed that the metabolic intermediate 5,6-dihydrox

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

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

148 ography with the radiotracer [(18)F]fluoro-l-DOPA to quantify striatal presynaptic dopamine synthesis

149 oups, and allows access to 6-[(18)F]fluoro-L-DOPA, 6-[(18)F]fluoro-m-tyrosine, and the translocator p

150 of genes aberrantly transcribed following l-DOPA treatment.

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

152 by excessive extracellular DA derived from L-DOPA, but potential involvement of DA reuptake in LID se

153 Furthermore, L-DOPA preferentially inhibits DA uptake in lesioned stria

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

155 tand how these striatal circuits change in l-DOPA-induced dyskinesias (LIDs).

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

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

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

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

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

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

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

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

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

165 The dopamine precursor levodopa (L-DOPA) increased the task-based learning rate and task pe

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

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

170 ivity were lower in PD models than normal; L-DOPA treatment restored these properties.

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

172 c neuromodulation by systemic injection of L-DOPA and Carbidopa (LDC) or by local application of DA i

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

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

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

176 The synthesis of a protected analog of l-DOPA demonstrates the utility of AHF for enantioselectiv

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

178 We argue that the need of l-DOPA for successful reproduction has driven D. sechellia

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

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

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

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

183 nesia is an incapacitating complication of L-DOPA therapy that affects most patients with Parkinson's

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

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

186 rons by ablating them before initiation of L-DOPA treatment and determining whether it decreases LID.

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

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

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

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

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

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

193 amine and primed with a chronic regimen of l-DOPA, SKF81297 or their vehicles.

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

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

196 red Parkinsonian nonhuman primate model of l-DOPA-induced dyskinesia (PD-LID).

197 The protein DREAM decreases development of L-DOPA-induced dyskinesia in mice and reduces L-DOPA-induc

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

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

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

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

202 enervation and pulsatile administration of L-DOPA.

203 hile maintaining the therapeutic effect of L-DOPA.

204 ring with the therapeutic motor effects of L-DOPA.

205 t compromising the therapeutic efficacy of L-DOPA.

206 dyskinesias, warranting discontinuation of l-DOPA.

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

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

209 e for the majority of patients who rely on L-DOPA to alleviate PD-related motor symptoms.

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

211 repinephrine, 3,4-dihydroxy-phenylalanine (L-DOPA), 3,4-dihydroxyphenylacetic acid (DOPAC), methyldop

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

213 ey received one of the following: placebo, L-DOPA (which increases dopamine levels in the brain), or

214 omedial striatum, +/-8-OH-DPAT potentiated l-DOPA-induced pERK; in the motor cortex, +/-8-OH-DPAT pot

215 or antagonist, with the dopamine precursor l-DOPA (25, 100, and 200 mg) or applied placebo medication

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

217 of dopamine by administering its precursor l-DOPA and/or dopamine D2-receptor agonists.

218 Administration of the dopamine precursor L-DOPA at a dose that replenished dopamine signaling in th

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

220 nal dopamine metabolism with the precursor l-DOPA, resuming oogenesis and stimulating egg production.

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

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

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

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

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

226 OPA-induced dyskinesia in mice and reduces L-DOPA-induced expression of FosB, phosphoacetylated histo

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

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

229 wn cells when incubated with the substrate l-DOPA.

230 6-hydroxydopamine lesions during long-term L-DOPA (25 mg/kg) treatment.

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

232 However, long-term L-DOPA treatment is complicated by eventual debilitating a

233 ting abnormal involuntary movements termed L-DOPA-induced dyskinesia (LID), a clinically significant

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

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

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

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

238 /2 in DMI + L-DOPA group compared with the L-DOPA- and DMI-alone groups.

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

240 and attenuates the behavioral response to l-DOPA and presynaptic and postsynaptic glutamate neurotra

241 s showed greater dyskinesia in response to l-DOPA and SKF81297 after repeated injections.

242 nt mice exhibit an exaggerated response to l-DOPA compared with control mice, suggesting that preserv

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

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

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

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

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

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

249 nergic neurons, the behavioral response to l-DOPA, and presynaptic and postsynaptic glutamate neurotr

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

251 without altering normal motor responses to L-DOPA.

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

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

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

255 's disease, serotonergic terminals take up L-DOPA and convert it to dopamine.

256 inson's disease are commonly treated using l-DOPA although long-term treatment usually causes debilit

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

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

259 essed more severe dyskinesia compared with L-DOPA alone over time.

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

261 cortex, +/-8-OH-DPAT potentiated pERK with l-DOPA or SKF81297.

262 -DPAT on pERK density in rats treated with l-DOPA or the D1 receptor agonist SKF81297.

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

264 roxydopamine and subsequently treated with L-DOPA to induce dyskinesia.

265 did not change in PD models, it fell with L-DOPA treatment.

266 ourse analysis (0-6 h after treatment with L-DOPA) identified an acute signature of 709 genes, among

267 Treatment with l-DOPA, a DA precursor, improved overall retinal and visua

268 CH23390 or their vehicles, and second with l-DOPA, SKF81297 or their vehicles.

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

270 ke in the DMI + L-DOPA group compared with L-DOPA-alone group in lesioned striatum.

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

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

273 ly dyskinetic animals after treatment with L-DOPA.

274 o change was observed after treatment with L-DOPA.

275 The symptoms of parkinsonism improved with l-DOPA; however, nearly all patients experienced early mot

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

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

278 iatal cells and are the most common cause of DOPA-responsive dystonia, a rare disease that classicall

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

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

281 g Gpc4-mutant cells expressed high levels of DOPA decarboxylase and the dopamine transporter, two mar

282 hypokinesia contrasting with a worsening of DOPA-unresponsive gait and balance disorders.

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

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

285 4-dihydroxyphenylalanine (DOPA) groups, pCB-(DOPA)4, were applied onto a paper-based sensor surface v

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

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

288 300 nM 1,2-dioleoyl-sn-glycero-3-phosphate (DOPA), but not the control 1,2-dioleoyl-sn-glycero-3-pho

289 g with 1, 2-dioleoyl-sn-glycero-3-phosphate (DOPA).

290 ions resulted in the association of a severe DOPA-responsive parkinsonism together with DOPA-unrespon

291 intoxicated with MPTP: they developed severe DOPA-responsive hypokinesia and tremor together with unr

292 It was anticipated that DOPA would mediate dehydration owing to its efficacy in

293 e functionalization, providing evidence that DOPA functionalization only occurs on the external surfa

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

295 a confirmed that the major ingredient of the DOPA-coated NPs was CDDP.

296 thogenic variants previously associated with DOPA-responsive dystonia (Q110X, V204I, K224R and M230I)

297 ated as aggregates, and then conjugated with DOPA to create stably dispersed colloids.

298 y) findings of four unrelated pedigrees with DOPA-responsive dystonia in which pathogenic GCH1 varian

299 e DOPA-responsive parkinsonism together with DOPA-unresponsive gait disorders.

300 ition to this, co-injection of tyramine with DOPA, the precursor of melanin, had a strong cumulative