ライフサイエンスコーパス: Parkinson disease

1 ins, and mutation in either domain can cause Parkinson disease.

2 ions confer an increased risk for developing Parkinson disease.

3 a constitutes an independent risk factor for Parkinson disease.

4 y and include LAMP3-selenium interaction and Parkinson disease.

5 of the retromer complex in the treatment of Parkinson disease.

6 sidase may prove useful for the treatment of Parkinson disease.

7 synuclein-positive aggregates, a hallmark of Parkinson disease.

8 olic profile in the putamen of patients with Parkinson disease.

9 he etiopathogenesis of Alzheimer disease and Parkinson disease.

10 a protective role in the cellular models of Parkinson disease.

11 Ambient air pollution exposures and risk of Parkinson disease.

12 e for its potential to be neuroprotective in Parkinson disease.

13 mpacta is a key neuropathological feature in Parkinson disease.

14 e microRNAs miR-19b, miR-29a, and miR-29c in Parkinson disease.

15 (CDNF) is a promising therapeutic agent for Parkinson disease.

16 s erythematosus, traumatic brain injury, and Parkinson disease.

17 e prevalence of alpha-synuclein pathology in Parkinson disease.

18 RK2), an ubiquitin ligase, cause early onset Parkinson disease.

19 onia, and off-state dystonia associated with Parkinson disease.

20 the defects in oxidative phosphorylation in Parkinson disease.

21 and treated (receiving dopaminergic therapy) Parkinson disease.

22 de a therapeutic benefit in animal models of Parkinson disease.

23 trastriatal serotonin transporter binding in Parkinson disease.

24 o determine whether they were diagnosed with Parkinson disease.

25 , causes protein misfolding and is linked to Parkinson disease.

26 use of creatine monohydrate in patients with Parkinson disease.

27 n the PINK1 gene cause early-onset recessive Parkinson disease.

28 ive proteinopathies, including Alzheimer and Parkinson disease.

29 tory and heterogeneous clinical phenotype of Parkinson disease.

30 re responsible for a common familial form of Parkinson disease.

31 7 through 2005 and had no prior diagnosis of Parkinson disease.

32 NVs in PARK2 are known to be associated with Parkinson disease.

33 ggested to contribute to the pathogenesis of Parkinson disease.

34 tions in the LRRK2 gene can cause late-onset Parkinson disease.

35 tant for future disease-modifying therapy in Parkinson disease.

36 processing and altered retinal morphology in Parkinson disease.

37 RAB39B resulted in pathologically confirmed Parkinson disease.

38 rotein alpha-synuclein (AS) is a hallmark of Parkinson disease.

39 RRK2 might contribute to the pathogenesis of Parkinson disease.

40 bute to the progressive neuropathogenesis of Parkinson disease.

41 of essential tremor and its relationship to Parkinson disease.

42 on and aggregate spreading in the context of Parkinson disease.

43 cer and neurodegenerative disorders, such as Parkinson disease.

44 ral neurodegenerative diseases, most notably Parkinson disease.

45 The main outcome was a diagnosis of Parkinson disease.

46 ve causes of dementia: Alzheimer disease and Parkinson disease.

47 ses on recent human (18)F-FDG PET studies in Parkinson disease.

48 ors to neurodegenerative disorders including Parkinson disease.

49 e important implication for the treatment of Parkinson disease.

50 ral efficacy in 6-OHDA lesioned rat model of Parkinson diseases.

51 diagnosis of a synucleinopathy (309 [67%] of Parkinson disease, 81 [17.6%] of dementia with Lewy bodi

52 cline therapy appeared to reduce the risk of Parkinson disease (adjusted IRR, 0.98 [95% CI, 0.97-0.99

53 ncentrated our review on multiple sclerosis, Parkinson disease, Alzheimer disease, and amyotrophic la

54 is, neuromyelitis optica spectrum disorders, Parkinson disease, Alzheimer disease, Huntington disease

55 (schizophrenia, affective disorders, stroke, Parkinson disease, amyotrophic lateral sclerosis, person

56 Methods Twenty patients with newly diagnosed Parkinson disease and 20 age-matched control subjects we

57 Two hundred sixteen patients with Parkinson disease and 204 control patients (patients wit

58 a is a major pathological process underlying Parkinson disease and a potential genetic mechanism of c

59 ce links neurodegenerative disorders such as Parkinson disease and Alzheimer disease with mitochondri

60 DJ-1 and SOD1, proteins involved in familial Parkinson disease and amyotrophic lateral sclerosis, res

61 nected to neurodegenerative diseases such as Parkinson disease and amyotrophic lateral sclerosis.

62 In idiopathic Parkinson disease and atypical parkinsonian disorders, c

63 vior disorder and antedates the diagnosis of Parkinson disease and dementia with Lewy bodies after 4.

64 ss the accuracy of diagnostic biomarkers for Parkinson disease and efficacy of L-DOPA therapy.

65 disorders, persistent pain syndromes or even Parkinson disease and multiple sclerosis).

66 ts component alleles have been implicated in Parkinson disease and narcolepsy.

67 its presence in Lewy bodies associated with Parkinson disease and neurofibrillary tangles observed i

68 rovide a novel therapeutic strategy for both Parkinson disease and neuronopathic forms of Gaucher dis

69 l disease-modifying therapy for treatment of Parkinson disease and neuronopathic Gaucher disease to i

70 impaired micturition and/or constipation in Parkinson disease and other alpha-synucleinopathies.

71 Parkinson disease and other neurodegenerative disorders

72 es, the neuron-associated aggregates seen in Parkinson disease and other neurodegenerative pathologie

73 Parkinson disease and other progressive neurodegenerativ

74 n), a key protein involved in development of Parkinson disease and other synucleinopathies.

75 Freezing of gait is a disabling symptom in Parkinson disease and related disorders, but the brain r

76 n genetic risk factor for the development of Parkinson disease and related disorders, implicating the

77 ynuclein, a protein present as aggregates in Parkinson disease and related synucleinopathies, were se

78 by alpha-synuclein oligomers, as observed in Parkinson disease and several other neurodegenerative di

79 to play a central role in the progression of Parkinson disease and strong evidence links chronic expo

80 terations can be detected in early stages of Parkinson disease and that the entire intracranial visua

81 therapeutics for treatment of Alzheimers and Parkinsons diseases and amyotrophic lateral sclerosis.

82 supranuclear palsy, 50 Alzheimer disease, 6 Parkinson disease, and 17 corticobasal syndrome patients

83 ng of gait is a poorly understood symptom of Parkinson disease, and can severely disrupt the locomoti

84 ith several diseases like diabetes, obesity, Parkinson disease, and certain types of cancers.

85 nked with neurodegeneration in Alzheimer and Parkinson disease, and many other pathologies.

86 Prion diseases, like Alzheimer's disease and Parkinson disease, are rapidly progressive neurodegenera

87 associated with neurologic disorders such as Parkinson disease-associated dementia and HIV-associated

88 Neurotoxicity of the Parkinson disease-associated pesticide ziram is synuclei

89 Here, we find that Parkinson disease-associated Vps35 variant, R524W, but n

90 alpha-syn accumulated within Lewy bodies in Parkinson disease brains is phosphorylated on serine 129

91 nase 2 (LRRK2) are a common genetic cause of Parkinson disease, but the mechanisms whereby LRRK2 is r

92 lein variants causative of familial forms of Parkinson disease can provide unique insights into the c

93 which is implicated in the familial form of Parkinson disease, complements the function of Hsp31 by

94 orsal striatum is the pathologic hallmark of Parkinson disease contributing to the primary motor symp

95 parkinsonism, dementia with Lewy bodies, and Parkinson disease dementia have increased mortality comp

96 of dementia with Lewy bodies, 55 [11.9%] of Parkinson disease dementia, and 16 [3.5%] of multiple sy

97 nts with pure autonomic failure will develop Parkinson disease, dementia with Lewy bodies, or multipl

98 ilable to slow or prevent the progression of Parkinson disease, despite its global prevalence and sig

99 ct of patients up to 20 years prior to their Parkinson disease diagnosis.

100 are the most common genetic risk factor for Parkinson disease, dopaminergic neurons were generated f

101 for a group of 8195 patients diagnosed with Parkinson disease during a 15-year period (January 1, 19

102 coronary heart disease, the hazard ratio of Parkinson disease during the 3-year follow-up period for

103 , 75.9 [10.2] years) received a diagnosis of Parkinson disease during the study period and 68053 indi

104 ascular AMD had a significantly lower 3-year Parkinson disease-free survival rate than comparison sub

105 psychiatric disorders, such as Alzheimer and Parkinson diseases, Gilles de la Tourette syndrome, and

106 This strategy to monitor cellular therapy of Parkinson disease has a high translational potential and

107 (hazard ratio, 3.86; 95% CI, 2.36-6.30), and Parkinson disease (hazard ratio, 1.75; 95% CI, 1.39-2.21

108 ial visual system changes of newly diagnosed Parkinson disease in drug-naive patients.

109 known to cause autosomal recessive cases of Parkinson disease in humans.

110 ent with thiazolidinediones and the onset of Parkinson disease in older individuals.

111 There was a 2-fold increased risk of Parkinson disease in patients classified as having ocula

112 dementia of any type, Alzheimer disease, and Parkinson disease in patients receiving blood transfusio

113 zards models to compare time to diagnosis of Parkinson disease in the propensity score-matched popula

114 ns were identified as putative biomarkers of Parkinson disease in the putamen of patients.

115 isorders including motor neurone disease and Parkinsons disease in addition to various types of cance

116 nct brain regions and associated symptoms in Parkinson disease, including cognitive decline.

117 We confirm that PINK1 mutations causing Parkinson disease interfere with the orchestration of se

118 The differentiation of idiopathic Parkinson disease (IPD) from multiple system atrophy (MS

119 ardiac sympathetic denervation in idiopathic Parkinson disease (IPD) using (11)C-hydroxyephedrine ((1

120 Idiopathic Parkinson disease is a common neurodegenerative disorder

121 Parkinson disease is a debilitating and incurable neurod

122 Our findings show that Parkinson disease is associated not only with the degene

123 Parkinson disease is associated with decreased activity

124 Familial Parkinson disease is associated with mutations in alpha-

125 Parkinson disease is associated with the progressive los

126 Currently, diagnosis of Parkinson disease is mainly based on clinical criteria c

127 The mortality among persons with Parkinson disease is only moderately increased compared

128 PARK2, a gene associated with Parkinson disease, is a tumor suppressor in human malign

129 re common in alpha-synucleinopathies such as Parkinson disease, Lewy body dementia, and multiple syst

130 We show that in individuals with Parkinson disease, Lewy body dementia, or multiple syste

131 affected by phosphorylation depending on the Parkinson disease-linked mutation.

132 ratio (log OR) = 0.15, P = 2 x 10(-12)) and Parkinson disease (log OR = -0.15, P = 1.6 x 10(-7)), am

133 impending alpha-synuclein disorder, such as Parkinson disease, multiple-system atrophy, or dementia

134 All the assessed autosomal dominant Parkinson disease mutations have significantly different

135 Among the known genetic risk factors for Parkinson disease, mutations in GBA1, the gene responsib

136 p region is found in the substantia nigra in Parkinson disease (n = 10) with respect to control cases

137 eveloped dementia with Lewy bodies (n = 13), Parkinson disease (n = 6), or multiple system atrophy (n

138 users had a hazard ratio for a diagnosis of Parkinson disease of 1.09 (95% confidence interval: 0.71

139 Those who phenoconverted to Parkinson disease or dementia with Lewy bodies had decre

140 Brains from patients with Parkinson disease or dementia with Lewy bodies show aggr

141 = 2.09), without significant differences in Parkinson disease or sleep disorders.

142 Because RBD is a prodromal syndrome of Parkinson disease (or related disorder), it represents a

143 Parkinson disease pathogenic mutations have an age-depen

144 f alpha-synuclein, a protein associated with Parkinson disease pathology.

145 re analyzed in 22 subthalamic nuclei from 13 Parkinson disease patients (57.5 +/- 5.9 years old, 4 fe

146 ived paraffin-embedded tissue blocks from 57 Parkinson disease patients (98 blocks) and 90 control su

147 een in the positivity rate between prodromal Parkinson disease patients and controls when using the a

148 after repeated levodopa (l-DOPA) exposure in Parkinson disease patients and remains one of the primar

149 Thirty-nine Parkinson disease patients contributed tissues obtained

150 d in the prodromal disease phase, whereas 18 Parkinson disease patients contributed tissues obtained

151 various gastrointestinal tract tissues from Parkinson disease patients in the prodromal phase.

152 Furthermore, Parkinson disease patients seem to have upregulation of

153 Parkinson disease patients showed statistically signific

154 directly comparing bicycling and walking in Parkinson disease patients with electrodes implanted in

155 ons complement prior neuroimaging studies in Parkinson disease patients, advancing our understanding

156 tralis OCT revealed retinal layer atrophy in Parkinson disease patients, especially in the inner laye

157 prior to debut of clinical motor symptoms in Parkinson disease patients.

158 n of which is found in post-mortem brains of Parkinson disease patients.

159 after repeated levodopa (l-DOPA) exposure in Parkinson disease patients.

160 es and neurites, the pathologic hallmarks of Parkinson disease (PD) and alpha-synucleinopathies.

161 ws for a highly accurate distinction between Parkinson disease (PD) and atypical parkinsonian syndrom

162 f the most common nonmotor manifestations of Parkinson disease (PD) and currently have only limited t

163 e investigated the polygenic architecture of Parkinson disease (PD) and have also explored the potent

164 lating cortical motor activity underlie both Parkinson disease (PD) and Huntington disease (HD).

165 cerebrospinal fluid (CSF) have been found in Parkinson disease (PD) and in PD dementia (PDD), but the

166 n abundant in presynaptic nerve terminals in Parkinson disease (PD) and is a major component of intra

167 Weight loss is common among persons with Parkinson disease (PD) and is associated with worse qual

168 nonmotor symptoms (NMSs) are common early in Parkinson disease (PD) and may be in part due to disease

169 function frequently occurs in the context of Parkinson disease (PD) and may precede onset of motor sy

170 l studies have reported the co-occurrence of Parkinson disease (PD) and melanoma.

171 structural brain connectome in patients with Parkinson disease (PD) and mild cognitive impairment (MC

172 Patients with Parkinson disease (PD) and mild cognitive impairment (MC

173 About one-third of patients with sporadic Parkinson disease (PD) and more than 40% of patients wit

174 The relationship between Parkinson disease (PD) and smoking has been examined in

175 Isolated dystonia and Parkinson disease (PD) are disorders of the basal gangli

176 rment in dementia with Lewy bodies (DLB) and Parkinson disease (PD) are multifactorial.

177 Cognitive impairments in Parkinson disease (PD) are thought to be caused in part

178 nce of cutaneous malignant melanoma (CMM) in Parkinson disease (PD) are unclear, but plausibly involv

179 visual hallucinations (VHs) in patients with Parkinson disease (PD) by analyzing whole-brain resting-

180 trends in the incidence of parkinsonism and Parkinson disease (PD) by comparing data from the first

181 Parkinson disease (PD) can be difficult to diagnose and

182 proaches to slow or block the progression of Parkinson disease (PD) do not exist.

183 recommendations on the medical management of Parkinson disease (PD) during Ramadan.

184 Detecting individuals at risk for Parkinson disease (PD) during the prodromal phase could

185 As many as 60% of patients with Parkinson disease (PD) experience psychosis, 80% develop

186 ons between higher body mass index (BMI) and Parkinson disease (PD) have been reported in observation

187 However, the few available studies on Parkinson disease (PD) have conflicting results, compris

188 a significantly higher propensity to develop Parkinson disease (PD) in comparison to the non-GD popul

189 on between the statin dosage and the risk of Parkinson disease (PD) in diabetic patients in Taiwan.

190 The revival of stereotactic surgery for Parkinson disease (PD) in the 1990s, with pallidotomy an

191 Parkinson disease (PD) is a complex neurodegenerative di

192 Parkinson disease (PD) is a neurodegenerative disorder p

193 Parkinson disease (PD) is a neurodegenerative disorder w

194 Parkinson disease (PD) is a progressive neurodegenerativ

195 Parkinson disease (PD) is an alpha-synucleinopathy resul

196 ment of levodopa-induced dyskinesia (LID) in Parkinson disease (PD) is an unmet need.

197 Previous studies demonstrated that Parkinson disease (PD) is associated with a decreased ac

198 There is increasing evidence that Parkinson disease (PD) is heterogeneous in its clinical

199 Importance: Parkinson disease (PD) is heterogeneous in symptom manif

200 ttern of regional metabolism associated with Parkinson disease (PD) is modulated by dopaminergic phar

201 Parkinson disease (PD) is second only to Alzheimer disea

202 t genetic risk factor for the development of Parkinson disease (PD) is the presence of a glucocerebro

203 Parkinson disease (PD) is the second most common neurode

204 goal of dopamine cell replacement therapy in Parkinson disease (PD) is to provide clinical benefit me

205 benefit of deep brain stimulation (DBS) for Parkinson disease (PD) may depend on connectivity betwee

206 dered protein alpha-synuclein (alpha-syn) in Parkinson disease (PD) pathogenesis has been well docume

207 tion into amyloid fibrils is associated with Parkinson disease (PD) pathogenesis.

208 rnover on damaged mitochondria is altered in Parkinson disease (PD) patient-derived fibroblasts conta

209 Ten Parkinson disease (PD) patients and 10 controls were inc

210 of autosomal-recessive early-onset forms of Parkinson disease (PD) remain to be elucidated.

211 er time in the incidence of parkinsonism and Parkinson disease (PD) remain uncertain.

212 igh prevalence of sleep-wake disturbances in Parkinson disease (PD) suggest a role of the circadian s

213 airment is a common and disabling problem in Parkinson disease (PD) that is not well understood and i

214 ed striatal presynaptic dopamine function in Parkinson disease (PD) was performed.

215 Patients with Parkinson disease (PD) who harbor LRRK2 G2019S mutations

216 double-blind trial in patients with advanced Parkinson disease (PD) who were randomly assigned to rec

217 ool for imaging the nigrostriatal pathway in Parkinson disease (PD) with PET.

218 ociated with an increased risk of developing Parkinson disease (PD), although the mechanisms by which

219 ld cognitive impairment (MCI), patients with Parkinson disease (PD), and young and older healthy volu

220 merging as a potentially relevant protein in Parkinson disease (PD), because it is a genetic modifier

221 ury (TBI) is thought to be a risk factor for Parkinson disease (PD), but results are conflicting.

222 teinopathies in a group of diseases, such as Parkinson disease (PD), dementia with Lewy bodies (DLB),

223 the most effective oral pharmacotherapy for Parkinson disease (PD), its use is often limited by wear

224 dered as a hallmark of sporadic and familial Parkinson disease (PD), little is known about the effect

225 In Parkinson disease (PD), mitochondrial dysfunction associ

226 The relationship between Parkinson disease (PD), PD with dementia (PDD), and deme

227 Compared with Parkinson disease (PD), potential genetic risk factors f

228 progressive supranuclear palsy (PSP) than in Parkinson disease (PD), we hypothesized that, in additio

229 icity are hallmarks of sporadic and familial Parkinson disease (PD), with accumulating evidence that

230 among patients with parkinsonism, including Parkinson disease (PD).

231 GBA gene mutations are the greatest cause of Parkinson disease (PD).

232 the effects of air pollution on the risk of Parkinson disease (PD).

233 e (GBA1) gene mutations increase the risk of Parkinson disease (PD).

234 ys a significant role in the pathogenesis of Parkinson disease (PD).

235 ammatory response plays an important role in Parkinson disease (PD).

236 o-controlled phase 2b trial in patients with Parkinson disease (PD).

237 demonstrated a growing genetic component in Parkinson disease (PD).

238 to toxic fibrils is a pathogenic hallmark of Parkinson disease (PD).

239 spectrum of predemented cognitive decline in Parkinson disease (PD).

240 iated with levodopa therapy in patients with Parkinson disease (PD).

241 AS)-copper complexes, and the development of Parkinson disease (PD).

242 LID) remains an unmet need for patients with Parkinson disease (PD).

243 closely examined as a possible treatment for Parkinson disease (PD).

244 repeat kinase 2 (LRRK2) is a common cause of Parkinson disease (PD).

245 disabling nonmotor symptoms in patients with Parkinson disease (PD).

246 in HTRA2/Omi/PARK13 have been implicated in Parkinson disease (PD).

247 ng and spreading the pathological process in Parkinson disease (PD).

248 g of gait (FOG) is a common axial symptom of Parkinson disease (PD).

249 rategy for slowing disability progression in Parkinson disease (PD).

250 d application of neuroimaging biomarkers for Parkinson disease (PD).

251 ished modality for the treatment of advanced Parkinson disease (PD).

252 ciation between immune-mediated diseases and Parkinson disease (PD).

253 Pain is a distressing symptom of Parkinson disease (PD).

254 degenerative disorders such as Alzheimer and Parkinson disease (PD).

255 by the SNCA gene, is strongly implicated in Parkinson disease (PD).

256 e clinically effective and cost-effective in Parkinson disease (PD).

257 st in neurodegenerative disorders, including Parkinson disease (PD); however, the contribution of ast

258 cus coeruleus, and ventral tegmental area in Parkinson disease (PD); the specific aims were (a) to st

259 and minimal adverse effects in patients with Parkinson disease (PD)?

260 s (n = 46) and patients meeting criteria for Parkinson disease (PD; n = 26).

261 everal neurodegenerative diseases, including Parkinsons disease (PD).

262 gic perikarya are differentially affected in Parkinsons disease (PD).

263 osed with Lewy-body diseases (LBDs; majority Parkinson disease [PD]; median survival time not reached

264 The IRs of Parkinson disease per 10000 person-years were 3.54 (95%

265 l Disorders and Stroke Exploratory Trials in Parkinson Disease program was established to promote dis

266 health-related quality of life (assessed by Parkinson Disease Questionnaire-39 and EuroQol-5D); adve

267 0.5 points; 95% CI, -0.7 to 1.7; P = .41) or Parkinson Disease Questionnaire-39 summary index (0.007

268 owed no difference in NEADL total score, but Parkinson Disease Questionnaire-39 summary index (diverg

269 ical improvement (motor score of the Unified Parkinson Disease Rating Scale [UPDRS]).

270 nt difference between the groups for Unified Parkinson Disease Rating Scale III.

271 elations to stage; disease duration; Unified Parkinson Disease Rating Scale motor score; posture inst

272 SD, 60 +/- 9 y; Hoehn and Yahr, 1-2; Unified Parkinson Disease Rating Scale motor, 18.9 +/- 6.7) and

273 JFK Coma Recovery Scale-Revised, the Unified Parkinson Disease Rating Scale, and the Burke-Fahn-Marsd

274 Among patients with Parkinson disease, RBD predicts a non-tremor-predominant

275 n real time to the intrinsically disordered, Parkinson disease related protein alpha-synuclein.

276 th factor-beta (TGF-beta) signaling promotes Parkinson disease-related pathologies and motor deficits

277 ific physical interaction exists between the Parkinson disease-related protein alpha-synuclein (alpha

278 ging the interactions of a natively unfolded Parkinson disease-related protein, alpha-synuclein (alph

279 Parkinson disease risk alleles in the MAPT (rs2942168; P

280 al layer thickness, duration of disease, and Parkinson disease severity.

281 patients with dementia with Lewy bodies and Parkinson disease shows that both diseases likely belong

282 gnaling pathway has therapeutic potential in Parkinson disease.SIGNIFICANCE STATEMENT We show that re

283 Results In the patients with Parkinson disease, significant alterations were found in

284 c symptoms, cognition and qUality of life in ParkinSon disease); SP0990) in treated Italian PD outpat

285 itivity was seen in 22 of 39 (56%) prodromal Parkinson disease subjects and 30 of 67 (45%) prodromal

286 h inflammation, increased risk of cancer and Parkinson disease, targeting C5aR1 may serve as a treatm

287 ness and safety for managing tremor-dominant Parkinson disease (TDPD) is unknown.

288 ssociated with a longer time to diagnosis of Parkinson disease than was sulfonylurea use, regardless

289 In patients with Parkinson disease, the correlation of the midbrain trace

290 In Parkinson disease, the protein alpha-synuclein (alphaSN)

291 adult onset conditions such as Alzheimer and Parkinson disease to neurodegenerative conditions of chi

292 Among patients with early and treated Parkinson disease, treatment with creatine monohydrate f

293 mon human disorders, including Alzheimer and Parkinson diseases, type II diabetes, and a number of sy

294 The adjusted IRR of Parkinson disease was 1.71 (95%, CI 1.52-1.92) in patien

295 A control group of 8195 patients without Parkinson disease was randomly matched with the Parkinso

296 In a Filipino woman with suspected Parkinson disease, we confirmed the presence of all chan

297 sponding estimates for Alzheimer disease and Parkinson disease were 0.99 (CI, 0.85 to 1.15) and 0.94

298 Parkinson disease with and without dementia (PDD and PD,

299 ies (hazard ratio, 3.94; 95% CI, 2.61-5.94), Parkinson disease with dementia (hazard ratio, 3.86; 95%

300 studies of an association between HTRA2 and Parkinson disease yielded conflicting results.