ライフサイエンスコーパス: substantia

1 brain regions-the frontal gyrus, the lateral substantia, and the medial substantia in PD patients.

2 owed clinically) showed prion protein in the substantia gelatinosa, spinothalamic tracts, posterior c

3 pioid-induced MOR internalization in the rat substantia gelatinosa.

4 yrus, the lateral substantia, and the medial substantia in PD patients.

5 ut to the magnocellular preoptic nucleus and substantia innominata (MCPO/SI) in mice and determined t

6 f glutamatergic and GABAergic neurons of the substantia innominata (SI) and magnocellular preoptic ar

7 BF, including the caudal globus pallidus and substantia innominata and moderate input from the horizo

8 gonal band, magnocellular preoptic area, and substantia innominata).

9 septum, bed nucleus of the stria terminalis, substantia innominata, various thalamic and hypothalamic

10 oradiography, we confirmed lower SV2A in the substantia nigra (-17%; p < 0.005) and nonsignificant fi

11 on disease group exhibited lower SV2A in the substantia nigra (-45%; p < 0.001), red nucleus (-31%; p

12 sterior thalamus (0.26% increase, P < .001), substantia nigra (0.25% increase, P = .01), red nucleus

13 ding potentials in the caudate, putamen, and substantia nigra (4.9, 4.9, and 1, respectively) were si

14 M-MRI signal in ventrolateral regions of the substantia nigra (area under the receiver operating char

15 nucleus (n = 13), globus pallidus (n = 13), substantia nigra (n = 13), posterior thalamus (n = 12),

16 ) and neuromelanin-containing neurons in the substantia nigra (off-target binding).

17 degeneration of dopaminergic neurons in the substantia nigra (SN) and affected the integrity of the

18 (PD), including dopaminergic neurons of the substantia nigra (SN) and cholinergic neurons of the dor

19 volved in T cell trafficking, in vivo in the substantia nigra (SN) and the serum of 1-methyl-4-phenyl

20 ndent dopaminergic (DA) neuronal loss in the substantia nigra (SN) and ventral tegmental area (VTA),

21 of N-glycans isolated from the striatum and substantia nigra (SN) can give an insight into the estab

22 models, STN DBS provides neuroprotection for substantia nigra (SN) dopamine neurons and increases BDN

23 CR attenuated the MPTP-induced loss of substantia nigra (SN) dopamine neurons and striatal dopa

24 ized pathologically by the selective loss of substantia nigra (SN) dopaminergic (DAergic) neurons.

25 ression levels and cell type patterns in the substantia nigra (SN) from 53 donors with and without PD

26 onsistent with the expression profile of the substantia nigra (SN) from PD patients, analyzed post mo

27 rons in the ventral tegmental area (VTA) and substantia nigra (SN) has been examined at multiple leve

28 Background The substantia nigra (SN) is suspected to be affected after

29 llular distribution of neutral lipids in the substantia nigra (SN) of Parkinson's disease (PD) patien

30 Dopamine neurons in the substantia nigra (SN) pars compacta are selectively lost

31 also differentiated DA neurons in the medial substantia nigra (SN) projecting either to dorsal or ven

32 DA neurons originating in the substantia nigra (SN) projecting to the dorsal striatum

33 The substantia nigra (SN) provides the largest dopaminergic

34 ulnerability of dopamine (DA) neurons in the substantia nigra (SN) to neurodegenerative stressors cau

35 man mutant alpha-synuclein (A53T) in the rat substantia nigra (SN) to produce degeneration of SN dopa

36 cal and functional organization of the human substantia nigra (SN) using diffusion and functional MRI

37 for the caudate, putamen, ventral striatum, substantia nigra (SN), and cerebellum were manually draw

38 n single-nuclei transcriptomic atlas for the substantia nigra (SN), generated by sequencing approxima

39 ng human alpha-syn fibril seeds into the rat substantia nigra (SN), in combination with adenoassociat

40 rest (ROIs): the dentate nucleus (DN), pons, substantia nigra (SN), pulvinar thalami, and globus pall

41 he switching neurons make projections to the substantia nigra (SN), ventral tegmental area (VTA) and

42 vels within dopaminergic (DA) neurons in the substantia nigra (SN), which may contribute to their sel

43 Rats were injected unilaterally, in the substantia nigra (SN), with AAV1/2-A53T-aSyn or control

44 umulates with age in dopamine neurons of the substantia nigra (SN).

45 ild-type alpha-syn unilaterally into the rat substantia nigra (SN).

46 eduction in GLAST/GLT-1 expression in murine substantia nigra (SN).

47 rons in the ventral tegmental area (VTA) and substantia nigra (SNc) encode reward prediction errors (

48 Iron concentrations were assessed in the substantia nigra (SNc), dentate and caudate nucleus, red

49 y loss of dopaminergic neurons (DaNs) in the substantia nigra (SNc), whereas DaNs in the neighboring

50 In particular, the dopaminergic substantia nigra (SNc)-related nigrostriatal pathway is

51 associated with increased iron levels in the substantia nigra (SNc).

52 robust inhibitory projections to the lateral substantia nigra (SNL) that contribute to appetitive and

53 hosphorylated alpha-synuclein in ipsilateral substantia nigra and adjacent to the injection site.

54 d better survival of dopaminergic neurons in substantia nigra and an increased number of microglia ex

55 oss of pigmented dopaminergic neurons in the substantia nigra and associated striatal deafferentation

56 degeneration of dopaminergic neurons in the substantia nigra and cholinergic neurons in the dorsal m

57 EAT1 is overexpressed in Parkinson's disease substantia nigra and confers drug-inducible neuroprotect

58 e the gene-gene regulatory structures in the substantia nigra and determine key regulators of the PD

59 DNER is highly expressed in substantia nigra and is an activator of the NOTCH1 pathw

60 ns in brain were between ADGRV1 and GRIK2 in substantia nigra and medullary inferior olivary nucleus,

61 (n = 15) and normal controls (n = 13) in the substantia nigra and putamen.

62 ngs using post-mortem histology of the human substantia nigra and radiotracer studies of the human st

63 e changes to PDE10A in striatoentopeduncular/substantia nigra and striatopallidal pathways might tigh

64 s that originates at least from two sources, substantia nigra and thalamic reticular nucleus.

65 her groups, and in globus pallidus, putamen, substantia nigra and the dentate nucleus compared to PD

66 d by the loss of dopaminergic neurons in the substantia nigra and the formation of Lewy body inclusio

67 oss of dopaminergic (DAergic) neurons in the substantia nigra and the gradual depletion of dopamine (

68 in neuromelanin-sensitive MRI signal in the substantia nigra and their relation to clinical scores o

69 art in the posterolateral motor areas of the substantia nigra and then progressed to more medial area

70 their projections to entopeduncular nucleus/substantia nigra and to external globus pallidus.

71 ctedly, this effect was not reflected in the substantia nigra and ventral tegmental area (SN/VTA), me

72 l dopamine-rich midbrain nuclei, such as the substantia nigra and ventral tegmental area, also exhibi

73 BPND in a midbrain region, encompassing the substantia nigra and ventral tegmental area, in 18 daily

74 The striatum as well as substantia nigra appeared normal and no loss of dopamine

75 was to validate free water in the posterior substantia nigra as a progression marker in Parkinson's

76 ore abundant in globus pallidus internus and substantia nigra at 6 months and remained so at 18 month

77 s post-surgery), and to the putamen plus the substantia nigra bilaterally in the second (8 years post

78 Degeneration of dopaminergic neurons in the substantia nigra causes the motor symptoms of Parkinson'

79 ns project to the ventral tegmental area and substantia nigra compacta but Nts(Dehy) neurons do not.

80 numerous cells of the ventral tegmental area/substantia nigra complex.

81 mitter in the striatum, while only few adult substantia nigra DA neurons have this capacity.

82 Moreover, direct stimulation of VTA or substantia nigra dopamine cell bodies failed to induce f

83 creased ventral tegmental area and decreased substantia nigra dopamine neuron population activity.

84 Substantia nigra dopamine neurons have been implicated i

85 otoxicity, as shown by increased survival of substantia nigra dopamine neurons, integrity of striatal

86 ysosomal dysfunction have been implicated in substantia nigra dopaminergic neurodegeneration in Parki

87 f dopamine inhibition.SIGNIFICANCE STATEMENT Substantia nigra dopaminergic neurons can be divided int

88 19S LRRK2 induces the robust degeneration of substantia nigra dopaminergic neurons, a pathological ha

89 TAAR1 prevents glutamate accumulation in the substantia nigra during hyperlocomotive states.

90 mic and transcriptomic data from putamen and substantia nigra from 117 human brains, interrogating re

91 Volumetric measurement of hyperintense substantia nigra from magnetization transfer-prepared T1

92 n particular the ictal increase in firing of substantia nigra GABAergic neurons.

93 ollowing the loss of dopamine neurons in the substantia nigra has been known for the last 50.

94 er-prepared T1-weighted MRI volumetry of the substantia nigra helped differentiate the stages of Park

95 Substantia nigra hyperechogenicity, olfactory loss, depr

96 e over 1 year in free water in the posterior substantia nigra in a large cohort of de novo patients w

97 ir axons to the targeted globus pallidus and substantia nigra in a time-dependent manner.

98 lterations in other brain regions beyond the substantia nigra in Parkinson's disease, multiple system

99 The ratio between the volume of the substantia nigra in patients with Parkinson's disease re

100 Moreover, overexpression of necdin in the substantia nigra in vivo of adult mice protects dopamine

101 nd tyramine reduced glutamate release in the substantia nigra in wild-type but not in TAAR1-KO mice.

102 that: (i) free water level in the posterior substantia nigra increased over 1 year in de novo Parkin

103 the anatomical and functional subdivision of substantia nigra into dorsal and ventral tiers and stria

104 I can depict a hyperintense subregion of the substantia nigra involved in the degeneration process of

105 demonstrate that free water in the posterior substantia nigra is a valid, progression imaging marker

106 ch as rotarod and treadmill tests, caused by substantia nigra lesioning in mice.

107 ritability of Parkinson's disease within the substantia nigra module.

108 mentary refers to 'Spatiotemporal changes in substantia nigra neuromelanin content in Parkinson's dis

109 Similarly, TRPC1(-/-) substantia nigra neurons showed increased L-type Ca(2+)

110 erexpression of human alpha-synuclein in the substantia nigra of aged (18 to 21-month-old) L444P Gba1

111 he midbrain of macaque monkeys, close to the substantia nigra of both sides.

112 d non-CpG sites in the entorhinal cortex and substantia nigra of control human postmortem brains, usi

113 we show that silencing netrin-1 in the adult substantia nigra of mice induces DCC cleavage and a sign

114 erely reduced in dopaminergic neurons of the substantia nigra of Parkinson's disease (PD) patients an

115 were found to be increased in the posterior substantia nigra of Parkinson's disease compared with co

116 s models have provided mixed findings in the substantia nigra of Parkinson's disease, but recent work

117 was increased in the anterior and posterior substantia nigra of Parkinson's disease, multiple system

118 longitudinally over 1 year in the posterior substantia nigra of Parkinson's disease.

119 hat RGMa is significantly upregulated in the substantia nigra of patients with Parkinson's disease.

120 ed with aggregated synuclein deposits in the substantia nigra of patients with Parkinson's disease.

121 complex I activity have been observed in the substantia nigra of PD patients, and loss of Parkin resu

122 romelanin-containing dopaminergic neurons in substantia nigra of PD patients.

123 lecule member a (RGMa) is upregulated in the substantia nigra of PD patients.

124 ate alpha-synuclein toxicity in vivo, in the substantia nigra of rats.

125 ntially expressed in striatoentopeducuncular/substantia nigra or striatopallidal pathways, respective

126 (mDA) or cortical glutamate neurons into the substantia nigra or striatum of a mouse PD model and fou

127 attenuate the activation of microglia in the substantia nigra par compacta of MPTP-treated mice.

128 neurons and dopaminergic neurons in the rat substantia nigra pars compact, increases the recruitment

129 eurons migrate to form the laterally-located substantia nigra pars compacta (SN) and medially-located

130 Dopamine neurons from the substantia nigra pars compacta (SNc) and ventral tegment

131 The rodent ventral tegmental area (VTA) and substantia nigra pars compacta (SNC) contain dopamine ne

132 Dopaminergic neurons (DAs) of the rodent substantia nigra pars compacta (SNc) display varied elec

133 e neurodegenerative disease characterized by substantia nigra pars compacta (SNc) dopamine (DA) neuro

134 Substantia nigra pars compacta (SNc) dopamine neurons an

135 TATEMENT Prior studies have established that substantia nigra pars compacta (SNc) dopamine neurons ar

136 to be a major factor underlying the loss of substantia nigra pars compacta (SNc) dopaminergic neuron

137 Burst spiking in substantia nigra pars compacta (SNc) dopaminergic neuron

138 on and behavior that depend on the firing of substantia nigra pars compacta (SNc) dopaminergic neuron

139 tion of a region homologous to the mammalian substantia nigra pars compacta (SNc) evokes increasing a

140 tanding how dopaminergic (DA) neurons of the substantia nigra pars compacta (SNc) govern movements re

141 regarding functional heterogeneity among the substantia nigra pars compacta (SNc) neurons.

142 Most dopaminergic neurons in the substantia nigra pars compacta (SNc), but not in ventral

143 ion between ventral tegmental area (VTA) and substantia nigra pars compacta (SNc), no clear evidence

144 ration of dopaminergic neurons (DaNs) of the substantia nigra pars compacta (SNc), resulting in the c

145 arkinson disease (PD)-related changes in the substantia nigra pars compacta (SNc), the key pathologic

146 It has been suggested that, in the substantia nigra pars compacta (SNc), the pacemaking rel

147 significant loss of dopamine neurons in the substantia nigra pars compacta (SNc).

148 erents from ventral tegmental area (VTA) and substantia nigra pars compacta (SNc).

149 and dendrites of dopamine neurons within the substantia nigra pars compacta (SNc).

150 ressive loss of dopamine (DA) neurons in the substantia nigra pars compacta (SNc).

151 TN DBS) protects dopaminergic neurons of the substantia nigra pars compacta (SNpc) against 6-OHDA and

152 Loss of dopaminergic (DA) neurons in the substantia nigra pars compacta (SNpc) and of noradrenerg

153 ic connections onto these neurons in the rat substantia nigra pars compacta (SNpc) and ventral tegmen

154 acterized by loss of dopamine neurons in the substantia nigra pars compacta (SNpc) and widespread agg

155 n travel to higher centers, compromising the substantia nigra pars compacta (SNpc) and, later, the ce

156 Neuronal loss in the substantia nigra pars compacta (SNpc) in Parkinson disea

157 Here we show that optogenetic activation of substantia nigra pars compacta (SNpc) neurons alleviates

158 ive dopaminergic (DA) neurons at the ventral substantia nigra pars compacta (SNpc) preferentially deg

159 tion of the dopaminergic (DA) neurons in the substantia nigra pars compacta (SNpc) remains to be answ

160 ng activity, reduced dopaminergic neurons in substantia nigra pars compacta (SNpc), and SNCA mice wer

161 significant loss of dopaminergic neurons in substantia nigra pars compacta (SNpc), and there was no

162 , loss of dopaminergic neurons (DANs) in the substantia nigra pars compacta (SNpc), decrease of dopam

163 euromelanin signal intensity loss within the substantia nigra pars compacta (SNpc), locus coeruleus,

164 n neuromelanin-containing cell levels in the substantia nigra pars compacta and nigrostriatal termina

165 diencephalic dopamine neurons located in the substantia nigra pars compacta and the ventral tegmental

166 Dopamine neurons in the substantia nigra pars compacta and ventral tegmental are

167 Midbrain dopaminergic (DA) neurons in the substantia nigra pars compacta and ventral tegmental are

168 e the interpeduncular nucleus, raphe nuclei, substantia nigra pars compacta and ventral tegmental are

169 Inhibiting both ventral tegmental area and substantia nigra pars compacta DA neurons in the post-re

170 n addition, in vivo recordings of identified substantia nigra pars compacta dopamine neurons in R1441

171 AIS length or distance from the soma in rat substantia nigra pars compacta dopaminergic neurons.

172 ted overexpression of alpha-synuclein in the substantia nigra pars compacta impacts visual processing

173 Degeneration of nigrostriatal neurons of substantia nigra pars compacta in Parkinson's disease re

174 c fibres from the ventral tegmental area and substantia nigra pars compacta innervate the majority of

175 degeneration of dopaminergic neurons in the substantia nigra pars compacta is the primary cause for

176 insight into how neuron subtypes outside the substantia nigra pars compacta may be compensating at a

177 ptor kinase type B (trkB) receptor occurs in substantia nigra pars compacta neurons and is required f

178 sed within vulnerable dopaminergic (DAergic) substantia nigra pars compacta neurons, only select down

179 In vivo data from the cortex and substantia nigra pars compacta of aged LRRK2 transgenic

180 ES and eotaxin were also up-regulated in the substantia nigra pars compacta of post-mortem PD brains

181 degeneration of dopaminergic neurons in the substantia nigra pars compacta portion of the brain.

182 iched brain fraction from frontal cortex and substantia nigra pars compacta tissue, isolated by sever

183 the degeneration of dopamine neurons of the substantia nigra pars compacta, a deficit in dopamine ne

184 d neurons and in dopaminergic neurons of the substantia nigra pars compacta, a susceptible brain regi

185 or abnormal protein accumulation within the substantia nigra pars compacta, suggesting that nigrostr

186 ally severe neuronal loss and gliosis in the substantia nigra pars compacta, without Lewy bodies.

187 eral amygdala, dorsal raphe nucleus, and the substantia nigra pars compacta.

188 preferential loss of dopamine neurons in the substantia nigra pars compacta.

189 d-phenylalanine was infused locally into the substantia nigra pars compacta.

190 (SNc), but not in ventral tegmental area or substantia nigra pars lateralis, consistently represente

191 s in STN, globus pallidus externa (GPe), and substantia nigra pars reticular (SNr), and disrupted bet

192 rvated the caudal-dorsal-lateral part of the substantia nigra pars reticulata (cdlSNr), directly or i

193 n the 25-40 Hz range in LFPs recorded in the substantia nigra pars reticulata (SNpr) and motor cortex

194 of studies have shown that inhibition of the substantia nigra pars reticulata (SNpr) attenuates seizu

195 ons from the pedunculopontine nucleus to the substantia nigra pars reticulata (SNr) act on muscarinic

196 ay, resulting in unbalanced responses in the substantia nigra pars reticulata (SNr) and suggesting a

197 the output of the basal ganglia through the substantia nigra pars reticulata (SNr) controls active a

198 l activation of CDt-derived terminals in the substantia nigra pars reticulata (SNr) inhibits SNr neur

199 odent basal ganglia (BG) output nucleus, the substantia nigra pars reticulata (SNr) is well positione

200 n of parvalbumin-positive (PV(+)) neurons in substantia nigra pars reticulata (SNR), accompanied with

201 observed to reach their midbrain target, the substantia nigra pars reticulata (SNr), at E14 in the mo

202 anglia GABAergic output in the midbrain, the substantia nigra pars reticulata (SNr), shows movement-r

203 Excitation of GABAergic cells in the substantia nigra pars reticulata (SNr), the main output

204 We recorded from the substantia nigra pars reticulata (SNR), the major basal

205 The substantia nigra pars reticulata (SNr), where the basal

206 unction by acting on 5-HT2C receptors in the substantia nigra pars reticulata (SNr), which in turn in

207 BA neurons, with ~50% of GABA neurons in the substantia nigra pars reticulata (SNr), ~30% in the VTA,

208 ors are coregulated by shared neurons in the substantia nigra pars reticulata (SNr).

209 a both the ipsilateral and the contralateral substantia nigra pars reticulata (SNr).

210 nd that excitation of GABAergic cells in the substantia nigra pars reticulata blocks signaled active

211 keeping constant the average firing rate of substantia nigra pars reticulata reduces the incidence o

212 r, the GABAergic output projections from the substantia nigra pars reticulata to the deep layers of t

213 proper GABAergic neuronal migration into the substantia nigra pars reticulata.

214 year increase in free water in the posterior substantia nigra predicts subsequent long-term progressi

215 he finding of increased NM-MRI signal in the substantia nigra provides additional insight into the pa

216 Conclusion In patients with stroke, greater substantia nigra R2*, likely reflective of greater iron

217 MTA1, we analyzed MTA1 and TH levels in the substantia nigra region of a large cohort of human brain

218 rhythmic activity of adult DA neurons in the substantia nigra region.

219 sh the physiological trajectory by which the substantia nigra reticulata (SNr) transitions from the h

220 y, immunohistochemistry analysis for MTA1 in substantia nigra sections revealed that 74.1% of the sam

221 Based on the aligned substantia nigra segmentations using a study-specific br

222 Increasing TGF-beta signaling in the substantia nigra through adeno-associated virus expressi

223 turally similar to those isolated from human substantia nigra tissues.

224 sed by a loss of dopaminergic input from the substantia nigra to the caudate nucleus and the putamen.

225 depression, anxiety, or hyperechogenicity on substantia nigra ultrasound.

226 cumulates in dopamine neurons of the VTA and substantia nigra via nifedipine-sensitive Ca(2+) channel

227 pose To evaluate quantitative measurement of substantia nigra volume by using MRI to support clinical

228 s before disease diagnosis, and 23.1% of the substantia nigra volume was lost at the time of diagnosi

229 internal reference was used for hyperintense substantia nigra volumetry normalized to intracranial vo

230 with CUD, greater D3R-related binding in the substantia nigra was associated with improved performanc

231 Neuronal loss of the substantia nigra was either absent or very mild in the p

232 emonstrated that free water in the posterior substantia nigra was elevated in Parkinson's disease com

233 The bilateral substantia nigra was evaluated by two neuroradiologists

234 potential for caudate nucleus, putamen, and substantia nigra was evaluated using the simplified refe

235 healthy control subjects, the volume of the substantia nigra was progressively reduced for increasin

236 the probability of a voxel belonging to the substantia nigra were calculated for patients with vario

237 ensive streaking and low signal intensity in substantia nigra were seen in two individuals.

238 esulted in Lewy pathology in the ipsilateral substantia nigra with significant reduction (-29.30%) of

239 led us to assess voxel-wise modifications of substantia nigra's morphology in vivo in humans, includi

240 acterized by loss of dopamine neurons in the substantia nigra(1).

241 men, nucleus accumbens, globus pallidus, and substantia nigra).

242 tyrosine hydroxylase-positive neurons in the substantia nigra, and attenuated the decrease of striata

243 d on GABAergic neurons of the basal ganglia, substantia nigra, and ventral tegmental area (VTA) where

244 f subcortical structures including striatum, substantia nigra, basal forebrain (BF), pedunculopontine

245 ly effective contacts included the thalamus, substantia nigra, brainstem and superior frontal gyrus.

246 ncluded the ethmoid sinus, clivus, meninges, substantia nigra, but not the basal ganglia or choroid p

247 Second, we analyzed expression in the human substantia nigra, comparing cell states in specific dono

248 S inhibited key brain regions, including the substantia nigra, entopeduncular nucleus, and nucleus ac

249 ted by RO5166017 when microinjected into the substantia nigra, infralimbic cortex, BLA, and CeA.

250 y, netrin-1 is highly expressed in the adult substantia nigra, leading us to investigate a role of th

251 In the substantia nigra, neurturin expression was detected in 9

252 riatal projections to entopeduncular nucleus/substantia nigra, preferentially expressing D1 receptors

253 For each voxel in the substantia nigra, probability map of controls, correlati

254 specifically in dopaminergic neurons of the substantia nigra, produced cataleptic behaviours associa

255 Substantia nigra, putamen, and cortical p11 protein leve

256 The identified modules were derived from the substantia nigra, putamen, frontal cortex, and white mat

257 d images was seen in the posterior thalamus, substantia nigra, red nucleus, cerebellar peduncle, coll

258 s, secreted by microglia, in the ipsilateral substantia nigra, the main region in the brain affected

259 that, in contrast to dopamine neurons in the substantia nigra, vagal motoneurons do not enhance their

260 a large number of CARTp-ir terminals in the substantia nigra, ventral tegmental area, periaqueductal

261 tein colocalizes with DA neurons in the male substantia nigra, where it regulates DA biosynthesis and

262 dicates that dopaminergic neurons in lateral substantia nigra, which innervate the sensorimotor stria

263 in the death of dopaminergic neurons in the substantia nigra, which is the root cause of dopamine de

264 with slower baseline gait speed (346 of 1807 substantia nigra-ventral tegmental area (SN-VTA) voxels,

265 gnaling, and loss of dopamine neurons in the substantia nigra.

266 ain, encompassing ventral tegmental area and substantia nigra.

267 rder involving dopaminergic neurons from the substantia nigra.

268 egions to dopamine-containing neurons of the substantia nigra.

269 ropagation from the most likely seed region, substantia nigra.

270 heral blood, frontal cortex, cerebellum, and substantia nigra.

271 including the caudate-putamen, striatum and substantia nigra.

272 of dopamine from both ventral tegmentum and substantia nigra.

273 ted with selective D-serine reduction in the substantia nigra.

274 orm gyrus, amygdala, striatum, pulvinar, and substantia nigra.

275 to the loss of dopaminergic neurons from the substantia nigra.

276 elective loss of dopaminergic neurons in the substantia nigra.

277 was measured in dopaminergic cells from the substantia nigra.

278 irectly (dMSNs) or indirectly (iMSNs) to the substantia nigra.

279 degeneration of dopaminergic neurons in the substantia nigra.

280 c model, the SVPE signal was detected in the substantia nigra.

281 yrosine hydroxylase (TH)-positive neurons of substantia nigra.

282 RD3-rich regions of the ventral pallidum and substantia nigra.

283 d by the loss of dopaminergic neurons in the substantia nigra.

284 sencephalic dopaminergic (DA) neurons in the substantia nigra.

285 lidus but decrease in entopeduncular nucleus/substantia nigra.

286 elective loss of dopaminergic neurons of the substantia nigra.

287 mpared with healthy controls, but not in the substantia nigra.

288 pigmented dopaminergic neuronal count in the substantia nigra.

289 of the basal Iba1-positive population in the substantia nigra.

290 rmined using a voxelwise analysis within the substantia nigra.

291 es were localized in distinct regions of the substantia nigra.

292 ources controls neuronal migrations into the substantia nigra.

293 ha-synuclein aggregates into the striatum or substantia nigra.

294 igher tracer binding in D3-rich regions: the substantia nigra/ventral tegmental area (SN/VTA) (+20%;

295 ocalization in brain areas projecting to the substantia nigra/ventral tegmental area.

296 l when isolated from postmortem PD patients' substantia nigra; and (b) leucine-rich repeat kinase 2 (

297 afferents to the ventral tegmental area and substantia nigra; the dopamine systems themselves; gluta

298 gation of alpha-synuclein (alpha-syn) in the substantia-nigra (SN).

299 .02 ppm +/- 0.03 and 21.7 sec(-1) +/- 5.26), substantia nigrae (case participants: 0.08 ppm +/- 0.06

300 06 ppm +/- 0.02 and 25.55 sec(-1) +/- 4.71), substantia nigrae (first MRI: 0.06 ppm +/- 0.06 and 28.2