ライフサイエンスコーパス: MPTP

1 MPTP (0-0.31 mg/kg) infused unilaterally via the interna

2 MPTP injections (1.5-2.1mg/kg) were made over a 5- to 7-

3 MPTP intoxication resulted in severe insomnia with delay

4 MPTP mice then received BDNF intranasally followed by mu

5 MPTP opening was directly regulated by gamma-secretase i

6 MPTP treatment also induced mitochondrial translocation

7 MPTP was determined using the calcein-cobalt technique.

8 MPTP-induced microglial activation and astrogliosis were

9 MPTP-induced reductions in ferroportin and elevations in

10 MPTP-lesioned primates were given systemic C3 (n = 8) or

11 MPTP-mediated toxicity in primary dopaminergic neurons w

12 it was not present in Macaca fascicularis (7 MPTP and 8 controls) with similar degree of MPTP-induced

13 ptide inhibitor P110 is neuroprotective in a MPTP animal model.

14 Inflammation induces aberrant MPTP opening, resulting in an increased apoptosis in con

15 Accordingly, MPTP/MPP(+) (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridin

16 nsitizes pancreatic mitochondria to activate MPTP, leading to mitochondrial failure; this makes the p

17 Ethanol and CCK activated MPTP through different mechanisms-ethanol by reducing th

18 administration of NTZ (50 mg/kg) in an acute MPTP mouse model of PD conferred significant protection

19 cise potently protects DA neurons from acute MPTP toxicity, suggesting that this simple lifestyle ele

20 persistent and progressive disease in acute MPTP-intoxicated mice.

21 fferent neurotoxic mouse models of PD, acute MPTP and sub-chronic LPS treatment, mRNA and protein lev

22 riatal dopaminergic pathway in the sub-acute MPTP mouse model of early-stage PD.

23 atal pathologies do not persist in the acute MPTP mouse model.

24 rain penetrant c-Abl inhibitor, in the acute MPTP-induced model of PD.

25 Additional MPTP injections resulted in the association of a severe

26 ) and Nrf2(-/-) background were administered MPTP.

27 ly, mice treated with allopregnanolone after MPTP lesion were able to perform at levels similar to th

28 striatum and improved gait dysfunction after MPTP administration.

29 s and lowered striatal dopamine levels after MPTP treatment, an effect that was reversed by selective

30 ke were reduced in the Bmal1(-/-) mice after MPTP treatment, suggesting that absence of Bmal1 may exa

31 was determined by stereological tests after MPTP intoxication in mice pretreated with either VIPR1 o

32 nd mitochondrial translocation in vivo after MPTP administration.

33 o (n = 7) for 2 months starting 1 week after MPTP.

34 for their abilities to protect mice against MPTP-induced neurodegeneration used to model Parkinson's

35 that are potentially neuroprotective against MPTP and that these factors change over time.

36 , these data suggest that protection against MPTP neurotoxicity may be mediated by alterations in iro

37 xercise provided complete protection against MPTP-induced neurotoxicity.

38 myeloid cells significantly protects against MPTP neurotoxicity and preserves striatal dopamine level

39 inergic cells and their terminations against MPTP insult, particularly in animals that developed few

40 e a key factor in protecting the VTA against MPTP-induced cell death, and that exogenous application

41 esides solely upon the soluble isoform in an MPTP-induced model of Parkinson's disease.

42 ue to follow this degeneration process in an MPTP-induced mouse model of PD.

43 murine microglial cell line BV2 cells in an MPTP-induced mouse model of PD.

44 en dysfunctional microglia of aging mice and MPTP exposure further inhibited astrocyte proneurogenic

45 by comparing glutamate levels in normal and MPTP-lesioned nonhuman primates (Macaca mulatta).

46 electron microscopic approach in normal and MPTP-treated monkeys.

47 of multisynaptic connectivity in normal and MPTP-treated monkeys; and 3) VGluT1- and vGluT2-positive

48 igra pars compacta (SNpc) against 6-OHDA and MPTP.

49 ndria exhibiting both IMAC-mediated RIRR and MPTP-mediated RIRR, diffusively coupled in a spatially e

50 ) lesion model of drug-induced rotation, and MPTP-treated non-human primate model.

51 neuron loss, and inflammatory phenotypes as MPTP-treated CX3CL1(-/-) mice, which received the GFP-ex

52 llular stress created by neurotoxins such as MPTP and 6-hydroxydopamine can upregulate VGluT2 in surv

53 dministration of SB216763 and atractyloside (MPTP opener) failed to abrogate a local cytoprotective G

54 1R inhibitor GW2580 significantly attenuated MPTP-induced CSF1R activation and Iba1-positive cell pro

55 a selective peptide inhibitor P110, blocked MPTP-induced Drp1 mitochondrial translocation and attenu

56 evented IOBA-NHC from cell death by blocking MPTP opening, DeltaPsim loss, Fas/FasL, and caspase acti

57 /-) mice were much more severely affected by MPTP than were those of their WT littermates.

58 nal damage and behavioral deficits caused by MPTP.

59 opening, or bistable dynamics facilitated by MPTP opening; 2), in a diffusively-coupled mitochondrial

60 effects of ethanol and CCK were mediated by MPTP because they were not observed in CypD(-/-) acinar

61 lly targeted CYP2D6 can efficiently catalyze MPTP-mimicking compounds, i.e. 2-methyl-1,2,3,4-tetrahyd

62 In PMA/alphaCD3-activated Jurkat T cells, MPTP opening and DeltaPsim loss were increased along wit

63 halted the disease progression in a chronic MPTP mouse model.

64 ow that neurodegeneration induced by chronic MPTP regimen is prevented by genetic deletion of SIRT2 i

65 In this study, using a classical MPTP animal PD model, we showed for the first time Drp1

66 maintaining the hydrogen bond; in contrast, MPTP*+ + tBu3PhOH maintains its conformation throughout

67 Furthermore, Nur77-deficient MPTP-treated mice displayed significantly reduced levels

68 PTP*+ < DeltaG()PPT*+ despite DeltaG degrees MPTP*+ > DeltaG degrees PPT*+.

69 oth experiment and calculations with DeltaG()MPTP*+ < DeltaG()PPT*+ despite DeltaG degrees MPTP*+ > D

70 Drp1 mitochondrial translocation diminished MPTP-induced p53, BAX and PUMA mitochondrial translocati

71 acids that occurs by a novel pathway during MPTP formation.

72 Genetic deficiency of the CIB1 gene enhances MPTP-induced neurotoxicity in dopaminergic neurons in CI

73 mutants lacking PGRN in microglia exhibited MPTP-induced phenotypes similar to Grn(-)/(-) mice.

74 Following MPTP or vehicle administration, mice ran on the treadmil

75 movement-related activity declined following MPTP but only marginally.

76 euron loss and behavioral deficits following MPTP intoxication.

77 nd its metabolites (DOPAC and HVA) following MPTP treatment as determined by HPLC method.

78 ost significant numbers of neurons following MPTP administration as compared to saline treated mice;

79 beled neurons/section in the SN-PC following MPTP, treadmill exercise leads to an increase of neurons

80 After controlling for MPTP-induced changes in motor performance, M1 activity r

81 cise also functionally protects neurons from MPTP-induced neurotoxicity.

82 release of dopamine and neuroprotection from MPTP toxicity in the VMAT2-overexpressing mice suggest t

83 inflammatory cytokine release resulting from MPTP exposure.

84 hydrogenase mRNA and activity resulting from MPTP were also found to be attenuated by DHB.

85 Our studies provide a novel LRRK2 gene-MPTP interaction PD mouse model, and a useful tool for f

86 The present study exposed monkeys to higher MPTP doses to produce significant parkinsonism and behav

87 In MPTP-treated mice, TTP expression increased and was co-l

88 The effects of allopregnanolone in MPTP-lesioned mice were more apparent in mice that under

89 -) mice was associated with an alteration in MPTP-mediated Ca(2+) efflux resulting in elevated levels

90 increased volume of their spine apparatus in MPTP-treated monkeys, suggesting an increased protein sy

91 rotect against nigrostriatal degeneration in MPTP-intoxicated mice.

92 okines, did not induce persistent disease in MPTP-insulted mice.

93 correlates with their protective efficacy in MPTP-mediated neurotoxicity.

94 continuous impairment of motor functions in MPTP-intoxicated mice.

95 ransmitters, and improved motor functions in MPTP-intoxicated mice.

96 Adding bilateral PPN lesions in MPTP-lesioned macaques induced dopamine-resistant gait a

97 s sensorimotor territory) was 26.1% lower in MPTP-treated parkinsonian monkeys than in controls.

98 ponses and protected dopaminergic neurons in MPTP-intoxicated mice, but at levels less than simvastat

99 FTI and GGTI also protected nigrostriata in MPTP-intoxicated mice.

100 e response of SVZ neuroprogenitors (NPCs) in MPTP-treated mice.

101 e components of the nigrostriatal pathway in MPTP-lesioned mice by measuring striatal dopamine levels

102 tal tract, improves the motor performance in MPTP-treated mice, and may serve as a therapeutic strate

103 yperdirect cortico-subthalamic projection in MPTP-treated parkinsonian monkeys.

104 acetic acid content (~29%), respectively, in MPTP-treated Bmal1(-/-) mice.

105 ese results extend prior positive results in MPTP models, are consistent with the results of a small

106 suggest that CIB1 plays a protective role in MPTP/MPP(+)-induced neurotoxicity by blocking ASK1-media

107 flammation and Wnt/beta-catenin signaling in MPTP-induced loss and repair of nigrostriatal dopaminerg

108 ation of neuronal cell bodies and termini in MPTP-intoxicated mice.

109 d exposure to environmental toxins including MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) are

110 hereas ER-Nix activates Bax/Bak-independent, MPTP-dependent necrosis.

111 In IOBA-NHC, TNFalpha, and IFNgamma induced MPTP opening, DeltaPsim loss, and increased cell apoptos

112 stimulated with thapsigargin, which induces MPTP formation by a direct effect on mitochondria, LDH a

113 e deletion of CD95 in DNs does not influence MPTP-induced neurodegeneration.

114 tochondrial calcium uptake but by inhibiting MPTP formation.

115 After transplantation into MPTP-lesioned mice, iDPs differentiated into DA neurons,

116 for 5 days and killed 7 days after the last MPTP injection.

117 conductance without altering inner membrane MPTP function, resulting in resistance to mitochondrial

118 NO suppresses APP translation in mouse MPTP models, explaining how elevated NO causes iron-depe

119 omoting NOX2 mRNA degradation in the MPP(+) /MPTP model of PD, suggesting that TTP could be a potenti

120 the parkinsonism-inducing neurotoxin MPP(+)/MPTP model that alpha-Synuclein (alpha-Syn), a presynapt

121 urons and several DA cell lines against MPP+/MPTP.

122 lly capable of activating the pro-neurotoxin MPTP and inducing neuronal damage, which is effectively

123 ia, and with the discovery of the neurotoxin MPTP a monkey model of PD had been developed.

124 tic inflammatory responses to the neurotoxin MPTP and reduced striatal dopamine turnover.

125 Furthermore, exposure to the neurotoxin MPTP depleted neurons in the ventrolateral VTA and resul

126 mates, and certain rodents by the neurotoxin MPTP.

127 lpha overexpression alone, in the absence of MPTP treatment, did not lead to cell loss in the SN or t

128 duction of parkinsonism by administration of MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) and

129 Chronic administration of MPTP induces lesion via apoptosis.

130 Intraperitoneal administrations of MPTP (a neurotoxin) were delivered to mice at regular in

131 on D-amino acids metabolism in the brain of MPTP-lesioned Macaca mulatta, and in the serum and cereb

132 vity of S1 and S2 terminals in VApc or CM of MPTP-treated monkeys, while the prevalence of "As" termi

133 matergic microcircuits in the VApc and CM of MPTP-treated parkinsonian monkeys.

134 ivo in the substantia nigra pars compacta of MPTP-intoxicated mice.

135 glia in the substantia nigra par compacta of MPTP-treated mice.

136 , can efficiently catalyze the conversion of MPTP to the toxic 1-methyl-4-phenylpyridinium ion.

137 f T cells into the nigra was found on 1 d of MPTP insult, T cell infiltration decreased afterward, be

138 MPTP and 8 controls) with similar degree of MPTP-induced nigrostriatal neurodegeneration; and (4) DA

139 striatum before and after a variable dose of MPTP in nonhuman primates.

140 LRRK2 transgenic mice to a sub-toxic dose of MPTP resulted in severe motor impairment, selective loss

141 e VTA to sustained exposure to a low dose of MPTP.

142 cillations, whereas the bistable dynamics of MPTP-mediated RIRR results in slow (0.1-2 microm/s) PsiM

143 urons in the substantia nigra independent of MPTP treatment, suggesting that microglial EP2 may influ

144 ase was developed using staged injections of MPTP.

145 , can efficiently catalyze the metabolism of MPTP to MPP(+), as shown with purified enzymes and also

146 discovery of the selective neurotoxicity of MPTP to dopamine cells, suspicion has focused on paraqua

147 uces a functional response in the outcome of MPTP-induced DAergic toxicity.

148 e of glial cells, catalyzes the oxidation of MPTP to the toxic 1-methyl-4-phenylpyridinium ion (MPP(+

149 a fundamental role in the physiopathology of MPTP-induced PD in a mouse model.

150 To examine the role of MPTP, we used ex vivo and in vivo models of pancreatitis

151 sitive and total cell numbers in the SNpc of MPTP-lesioned mice, even though this did not increase st

152 igand binding was evident in the striatum of MPTP lesioned animals as compared with the control group

153 caspase activities with a minimal effect on MPTP.

154 s exposure to neurotoxins, such as 6-OHDA or MPTP, that model certain aspects of Parkinson's disease

155 nistration, mice were treated with saline or MPTP.

156 or 3months prior to treatment with saline or MPTP.

157 or 3months prior to treatment with saline or MPTP.

158 MCU-mediated mitochondrial calcium overload, MPTP formation, and necrotic cell death.

159 ted the effects of ethanol on the pancreatic MPTP, the mechanisms of these effects, and their role in

160 wo toxin models of Parkinson's disease (PD), MPTP and paraquat, in young animals, its prolonged eleva

161 hance outer membrane permeability, permitted MPTP-dependent mitochondrial swelling and restored necro

162 -(pyrid-2-yl)-10-methyl-10H-phenothiazinium (MPTP*+).

163 c loss following 1-methyl-4-phenylpyridinium/MPTP treatment, in vitro and in vivo.

164 mitochondrial permeability transition pore (MPTP) causes loss of the mitochondrial membrane potentia

165 mitochondrial permeability transition pore (MPTP) causes loss of the mitochondrial membrane potentia

166 mitochondrial permeability transition pore (MPTP) causes mitochondrial dysfunction and necrosis in a

167 mitochondrial permeability transition pore (MPTP) formation, lactate dehydrogenase (LDH) release, an

168 mitochondrial permeability transition pore (MPTP) opening.

169 mitochondrial permeability transition pore (MPTP) via cyclophilin D and p53 as mechanisms of EPHOSS.

170 mitochondrial permeability transition pore (MPTP) was affected in PS1 mutants, being accelerated in

171 Mitochondrial Permeability Transition Pore (MPTP), is formed within the c-subunit ring of the ATP sy

172 mitochondrial permeability transition pore (MPTP).

173 mitochondrial permeability transition pore (MPTP).

174 mitochondrial permeability transition pore (MPTP).

175 mitochondrial permeability transition pore (MPTP).

176 mitochondrial permeability transition pore (MPTP).

177 mitochondria permeability transition pores (MPTP).

178 +) uniporter (MCU) regulator, also prevented MPTP formation and arachidonic acid release induced by A

179 ting myeloid cells, and efficiently prevents MPTP-induced DN death.

180 We used the progressively MPTP-intoxicated monkey model that expresses recovery fr

181 onal and unique benefit in mice who received MPTP.

182 a knockdown or GSK-3beta antagonism reversed MPTP-induced neurogenic impairment ex vivo/in vitro or i

183 nt sensitivity to damage induced by systemic MPTP treatment.

184 4-(2'-methylphenyl)-1,2,3,6-tetrahydrophine (MPTP), mice lacking PGRN (Grn(-)/(-)) showed more neuron

185 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridin (MPTP)-induced neurodegeneration using tissue-specific de

186 -methyl-4-phenyl-1,2,4,5-tetrahydropyridine (MPTP)-treated mice resulted in obvious motor functional

187 -methyl-4-phenyl-1,2,5,6 tetrahydropyridine (MPTP) treatment.

188 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) administration affected extracellular cortical glu

189 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and dyskinetic with levodopa.

190 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) animal model of PD.

191 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) caused dopaminergic cell death.

192 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) exposure in nonhuman primates.

193 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in the adult mouse.

194 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) into non-human primates causes injury to the nigro

195 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) intoxication to model PD in mice.

196 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) intoxication to render them parkinsonian and then

197 -Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) is a dopaminergic neurotoxin that replicates most

198 -Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) is a neurotoxic side product formed in the chemica

199 thyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP) model of Parkinson's disease (PD).

200 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) model of Parkinson's disease.

201 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) model of PD to investigate the possible use of LXR

202 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) model of PD.

203 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model is the most widely used animal model f

204 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of Parkinson's disease.

205 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) of PD were used.

206 -methyl 4-phenyl 1,2,3,6-tetrahydropyridine (MPTP) toxicity.

207 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) treatment in vivo, Nur77 expression in the nigrost

208 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), abnormal low beta (8-15 Hz) spiking and local fie

209 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), as measured by reduced dopamine terminal damage a

210 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), leading to parkin inactivation, accumulation of t

211 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), producing bilateral degeneration of the nigrostri

212 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced bilateral nigrostriatal dopaminergic lesio

213 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced mouse model of PD and that it can also inh

214 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced nigral dopaminergic cell loss and up-regul

215 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced Parkinsonism in nonhuman primates.

216 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD mouse model.

217 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD.

218 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-intoxicated mice where it inhibits parkin through

219 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-intoxicated mice.

220 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-intoxicated monkeys (when motor symptoms are less

221 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-lesioned mice.

222 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-lesioned mouse.

223 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-mediated cell death of dopaminergic neurons in the

224 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-mimicking chemicals that are metabolic conversion

225 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-rendered Parkinsonian nonhuman primate model of l-

226 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated monkeys, as well as in some electrophysiol

227 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated monkeys.

228 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated nonhuman primates.

229 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP).

230 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP).

231 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP).

232 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP).

233 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP/MPP+) in a mouse model of PD.

234 We found that MPTP treatment increases D-aspartate and D-serine in the

235 It was also noted that MPTP treated mice to which allopregnanolone was administ

236 In conclusion, our findings suggest that MPTP induced PD in mouse model is appropriate to follow

237 The MPTP inhibitor cyclosporin A protects mouse bone marrow

238 or function despite administration after the MPTP injury process had begun.

239 Combined inhibition of caspases and the MPTP fully protected against Nix-mediated cell death.

240 mediators, and significantly attenuated the MPTP-induced loss of dopamine neurons and motor behavior

241 CR attenuated the MPTP-induced loss of substantia nigra (SN) dopamine neur

242 By contrast, the MPTP-NIr group developed much less clinical and behavior

243 by suggesting a physiologic function for the MPTP.

244 D on the development of the phenotype in the MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridinen) mod

245 All monkeys in the MPTP group developed severe clinical and behavioral impa

246 , and as a result, enhances apoptosis in the MPTP model of PD.

247 amine metabolism, and motor phenotype in the MPTP mouse model of parkinsonism.

248 Furthermore, juglone treatment in the MPTP mouse model of PD suppressed Pin1 levels and improv

249 persistent nigrostriatal pathologies in the MPTP mouse model, and that targeting these factors may h

250 down the progression of neuronal loss in the MPTP mouse model.

251 APP-overexpressing mice are protected in the MPTP PD model.

252 Further, in the MPTP-induced neurotoxin model of PD in cultured cells an

253 r to 1-methyl-4-phenylpyridinium (MPP+), the MPTP metabolite responsible for its neurotoxicity.

254 cell death, the physiologic function of the MPTP is largely unknown.

255 molecular identity of the components of the MPTP remains unknown.

256 in cyclophilin D (CypD), a component of the MPTP, are resistant to MPTP opening, loss of DeltaPsim,

257 tion waves; and 3), the slow velocity of the MPTP-mediated depolarization wave is related to competit

258 ilitating outer membrane permeability of the MPTP.

259 peptidyl-prolyl isomerase that regulates the MPTP and is a drug target for AP.

260 Our data predict that the MPTP is an inner membrane regulated process, although in

261 These findings suggest that the MPTP maintains homeostatic mitochondrial Ca(2+) levels t

262 motor cortex on the side ipsilateral to the MPTP-lesion.

263 re inconsistent with those attributed to the MPTP.

264 dysfunction in female mice treated with the MPTP, as a model of parkinsonism.

265 dria which may or may not be linked with the MPTP.

266 immunocytes or natural Tregs administered to MPTP mice attenuated microglial inflammatory responses a

267 ns from agonist-treated mice administered to MPTP-intoxicated animals.

268 rm provides no neuroprotective capability to MPTP-induced pathologies, exhibiting similar motor coord

269 ost significant numbers of DA neurons due to MPTP toxicity; however, the 2/3 running group demonstrat

270 se in TH-labeled neurons in the SN-PC due to MPTP will be partially reversed by treadmill exercise, l

271 que transcriptional response when exposed to MPTP, a neurotoxin able to mimic the selective cell loss

272 icient for neuroprotection after exposure to MPTP.

273 Administration of the LXR agonist GW3965 to MPTP-treated WT mice protected against loss of dopaminer

274 eptibility of LRRK2 KO and wild-type mice to MPTP.

275 ctive vulnerability of Grn(-)/(-) neurons to MPTP, but rather to an increased microglial inflammatory

276 role in the susceptibility of DA neurons to MPTP, we generated LRRK2 knock-out (KO) mice lacking the

277 ired for the susceptibility of DA neurons to MPTP.

278 ), a component of the MPTP, are resistant to MPTP opening, loss of DeltaPsim, and necrosis.

279 h are devoid of T cells and are resistant to MPTP-induced neurodegeneration, become susceptible to MP

280 ression of 148 genes as an early response to MPTP and 113 genes as a late response to MPTP toxicity.

281 and subsequent neurotoxicity in response to MPTP intoxication.

282 to MPTP and 113 genes as a late response to MPTP toxicity.

283 tionally increased in the VTA in response to MPTP.

284 drion-targeted CYP2D6 were more sensitive to MPTP-mediated mitochondrial respiratory dysfunction and

285 -1alpha also led to increased sensitivity to MPTP-induced death of Th+ neurons.

286 vels of Pitx3 and enhances susceptibility to MPTP.

287 ced neurodegeneration, become susceptible to MPTP-induced loss of dopaminergic neurons when reconstit

288 ly, D3R-deficient mice become susceptible to MPTP-induced neurodegeneration and microglial activation

289 a new model of PD that combines a sub-toxic MPTP insult to the G2019S-LRRK2 mutation.

290 pronounced effects in VIPR2 agonist-treated, MPTP-intoxicated mice.

291 Unilateral MPTP-administration rendered the animals with hemiparkin

292 PRP activity was elevated in the untreated MPTP hemispheres relative to those of the normal control

293 activity remained unchanged in the untreated MPTP hemispheres versus the sham-operated hemispheres.

294 Importantly, in vivo studies using MPTP, LPS, or 6-OHDA models revealed a greater attenuati

295 lar results in aged monkeys intoxicated with MPTP: they developed severe DOPA-responsive hypokinesia

296 hydroxylase expression after lesioning with MPTP.

297 astrocyte activation, whereas nTg mice with MPTP exposure showed no deficits.

298 al mouse and after damage of DA neurons with MPTP.

299 Pre-exposure to CD to mice treated with MPTP resulted in an exacerbation of motor deficit and a

300 d nigrostriatal damage when compared with WT MPTP-treated controls.