ライフサイエンスコーパス: Parkinson disease

1 and K(i) change found significant effects of Parkinson disease.

2 iece, we discuss progress in the genetics of Parkinson disease.

3 ic acid were associated with a lower risk of Parkinson disease.

4 ve diseases, including Alzheimer disease and Parkinson disease.

5 agus nerve analogously to alpha-synuclein in Parkinson disease.

6 ry outcome was a new diagnosis of idiopathic Parkinson disease.

7 associated with the subsequent diagnosis of Parkinson disease.

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

9 n and are associated with the early onset of Parkinson Disease.

10 ral neurodegenerative diseases, most notably Parkinson disease.

11 The main outcome was a diagnosis of Parkinson disease.

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

13 ors to neurodegenerative disorders including Parkinson disease.

14 igra involved in the degeneration process of Parkinson disease.

15 e important implication for the treatment of Parkinson disease.

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

17 ions confer an increased risk for developing Parkinson disease.

18 ) gene are the most common cause of familial Parkinson disease.

19 a constitutes an independent risk factor for Parkinson disease.

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

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

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

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

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

25 he etiopathogenesis of Alzheimer disease and Parkinson disease.

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

27 Ambient air pollution exposures and risk of Parkinson disease.

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

29 mpacta is a key neuropathological feature in Parkinson disease.

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

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

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

33 ong been an attractive prospect for treating Parkinson disease.

34 re than 6 million individuals worldwide have Parkinson disease.

35 aSN) is an important histological feature of Parkinson disease.

36 ain stimulation (DBS) in three patients with Parkinson disease.

37 to support clinical diagnosis and staging of Parkinson disease.

38 tia nigra helped differentiate the stages of Parkinson disease.

39 s thought to underlie disease progression in Parkinson disease.

40 gger for excessive inflammatory responses in Parkinson disease.

41 sleep relates to slower motor progression in Parkinson disease.

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

43 psychosis (16 patients, 16 controls), and in Parkinson disease (16 patients, 16 controls).

44 our institution (n(total) = 482 patients; n(Parkinson disease) = 303; n(dystonia) = 64; n(tremor) =

45 alcohol-use disorder (34%, P = 0.00084) and Parkinson disease (34%, P = 0.0032) than in their corres

46 Individuals with mild motor-predominant Parkinson disease (49%-53% of individuals with Parkinson

47 neuron-specific protein PGP9.5 (PGP9.5) and Parkinson disease 5 (PARK5), a DUB active in neurons tha

48 ; 19 men), and 31 participants with advanced Parkinson disease (60 years +/- 9; 16 women).

49 11; 11 women), 29 participants with de novo Parkinson disease (64 years +/- 10; 19 men), and 31 part

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

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

52 d October 2015 for participants with de novo Parkinson disease, advanced Parkinson disease, and healt

53 isease, are a common genetic risk factor for Parkinson disease, although the penetrance is low.

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

55 brovascular risk factors are associated with Parkinson disease, an effect comparable to their associa

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

57 ,531 (1.5%) participants were diagnosed with Parkinson disease and 81,974 (7.9%) were diagnosed with

58 le sclerosis, amyotrophic lateral sclerosis, Parkinson disease and Alzheimer disease.

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

60 (PSP) and Lewy body disorders, which include Parkinson disease and dementia with Lewy bodies, is ofte

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

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

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

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

65 Parkinson disease and other neurodegenerative disorders

66 Parkinson disease and other progressive neurodegenerativ

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

68 r control, as evidenced by its importance in Parkinson Disease and related disorders.

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

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

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

72 r accurate and early differentiation between Parkinson disease and the various forms of atypical park

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

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

75 nts with de novo Parkinson disease, advanced Parkinson disease, and healthy control participants.

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

77 tau in Alzheimer disease, alpha-synuclein in Parkinson disease, and TAR DNA-binding protein 43 in amy

78 aling of the VGLUT3-mGluR5 axis is linked to Parkinson disease, anxiety disorders, and drug addiction

79 s pathologies including, but not limited to, Parkinson disease, anxiety disorders, and drug addiction

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

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

82 Parkinson disease-associated mutations within the GTPase

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

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

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

86 euron function, survival and degeneration in Parkinson disease', by Lee et al. (doi:10.1093/brain/awa

87 pathology and dysregulation of monocytes in Parkinson disease can act together to induce excessive i

88 role of systemic inflammation on the risk of Parkinson disease compared to amyotrophic lateral sclero

89 inson disease, dementia with Lewy bodies, or Parkinson disease dementia (OR = 3.70, 95% CI: 2.07-6.62

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

91 nson disease, dementia with Lewy bodies, and Parkinson disease dementia) compared with age- and sex-m

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

93 ith Lewy bodies than in Parkinson disease or Parkinson disease dementia, and in men than in women, bu

94 ivastigmine can be used to treat symptomatic Parkinson disease dementia.

95 ients who developed alpha-synucleinopathies (Parkinson disease, dementia with Lewy bodies, and Parkin

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

97 .0004), and higher in men than in women with Parkinson disease, dementia with Lewy bodies, or Parkins

98 ividuals and patients with BP with preceding Parkinson disease, dementia, and stroke.

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

103 DBS is a standard of care in Parkinson disease, essential tremor and dystonia, and is

104 current limitations and the broader range of Parkinson disease features that dopamine cell replacemen

105 15, P < .001) and participants with de novo Parkinson disease from those with advanced Parkinson dis

106 of PHGDH regulation, demonstrating that the Parkinson disease gene and tumor suppressor Parkin bound

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

108 Post hoc analyses revealed that the Parkinson disease group exhibited lower SV2A in the subs

109 Parkinson disease has multiple disease variants with dif

110 derived cell transplants in individuals with Parkinson disease have been variable, in part owing to t

111 ired, now that gene-targeting approaches for Parkinson disease have reached the clinical trial stage.

112 rkinson disease (49%-53% of individuals with Parkinson disease) have mild symptoms, a good response t

113 alignant subtype (9%-16% of individuals with Parkinson disease) have prominent early motor and nonmot

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

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

116 nstem nuclei involved in the pathogenesis of Parkinson disease in living patients.

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

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

119 ratios of amyotrophic lateral sclerosis and Parkinson disease in relation to leukocytes, immunoglobu

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

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

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

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

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

125 Idiopathic Parkinson disease is a common neurodegenerative disorder

126 Parkinson disease is a debilitating and incurable neurod

127 Parkinson disease is a heterogeneous disease with rapidl

128 Diagnosis of Parkinson disease is based on history and examination.

129 Parkinson disease is characterized by motor and nonmotor

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

131 Parkinson disease is the most common form of parkinsonis

132 owever, the importance of slow-wave sleep in Parkinson disease is unknown.

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

134 alpha-synuclein pathology is the hallmark of Parkinson disease, it has not been investigated whether

135 nism, a group of neurological disorders with Parkinson disease-like movement problems such as rigidit

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

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

138 Palliative care is part of Parkinson disease management.

139 s now known that the pathological process in Parkinson disease may begin decades before the clinical

140 participants from participants with advanced Parkinson disease (mean difference for ipsilateral side,

141 participants from participants with de novo Parkinson disease (mean difference for ipsilateral side,

142 o Parkinson disease from those with advanced Parkinson disease (mean difference for ipsilateral side,

143 (2016) Genetics in Parkinson disease: Mendelian versus non-Mendelian inheri

144 yneuropathy, diseases of myoneural junction, Parkinson disease, multiple sclerosis, central nervous s

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

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

147 utoradiography in an independent sample with Parkinson disease (n = 15) and normal controls (n = 13)

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

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

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

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

152 P diagnosis and that patients with preceding Parkinson disease or dementia, but not stroke, are signi

153 develop in dementia with Lewy bodies than in Parkinson disease or Parkinson disease dementia, and in

154 higher in dementia with Lewy bodies than in Parkinson disease (OR = 2.57, 95% CI: 1.50-4.40, p = 0.0

155 nt in neurological disorders such as stroke, Parkinson disease, or Huntington disease.

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

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

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

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

160 Parkinson disease patients appeared to have lower levels

161 Most importantly, monocytes from Parkinson disease patients are dysregulated and hyperact

162 t evidence suggests that immune responses in Parkinson disease patients are dysregulated, leading to

163 Thirty-nine Parkinson disease patients contributed tissues obtained

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

165 Although LRRK2-related Parkinson disease patients have a heightened risk of cer

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

167 Blood extracellular vesicles from Parkinson disease patients induce a stronger activation

168 Data mining of the brain transcriptome in Parkinson disease patients supported CR4 as an active al

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

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

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

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

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

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

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

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

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

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

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

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

181 tau) in many neurologic disorders, including Parkinson disease (PD) and related parkinsonisms, Alzhei

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

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

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

185 A recent study found a decreased risk of Parkinson disease (PD) associated with the beta2 adrener

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

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

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

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

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

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

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

193 Parkinson disease (PD) has useful symptomatic treatments

194 Alterations of the gut microbiome in Parkinson disease (PD) have been repeatedly demonstrated

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

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

197 le genome-wide association studies (GWAS) in Parkinson disease (PD) have identified a signal at chrom

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

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

200 served to be associated with a lower risk of Parkinson disease (PD) in previous epidemiologic studies

201 Parkinson disease (PD) is a devastating, largely nonfami

202 Parkinson disease (PD) is a neurodegenerative disorder p

203 Parkinson disease (PD) is a neurodegenerative disorder w

204 Parkinson disease (PD) is a progressive neurodegenerativ

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

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

207 A major contributor to dementia in Parkinson disease (PD) is degeneration of the cholinergi

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

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

210 the substantia nigra pars compacta (SNpc) in Parkinson disease (PD) is not uniform, as dopamine neuro

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

212 Parkinson disease (PD) is the most common neurodegenerat

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

214 efficacy of deep brain stimulation (DBS) for Parkinson disease (PD) is well established for up to 1 o

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

216 Freezing of gait (FOG) in Parkinson disease (PD) often occurs during steering of g

217 he demonstrated implication of the retina in Parkinson disease (PD) pathology and the importance of d

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

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

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

221 We studied 22 individuals [8 Stroke and 14 Parkinson Disease (PD) subjects aged between 41 and 75 y

222 ual hit hypothesis about the pathogenesis of Parkinson disease (PD) suggests that the brainstem is a

223 Parkinson disease (PD) treatment options have convention

224 s Participants with essential tremor (ET) or Parkinson disease (PD) undergoing thalamotomy were prosp

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

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

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

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

229 have signs and symptoms overlapping those of Parkinson disease (PD), complicating their clinical diag

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

231 mutations, the most common genetic cause of Parkinson disease (PD), display incomplete penetrance, i

232 In Parkinson disease (PD), for example, oestrogens can infl

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

234 In Parkinson disease (PD), mitochondrial dysfunction associ

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

236 Parkinson disease (PD), the most common movement disorde

237 Typically, in Parkinson disease (PD), there is a differential loss of

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

239 niques have shown promise in capturing early Parkinson disease (PD)-related changes in the substantia

240 isorders, such as Alzheimer disease (AD) and Parkinson disease (PD).

241 r disease, increase the risk and severity of Parkinson disease (PD).

242 seases, including Alzheimer disease (AD) and Parkinson disease (PD).

243 kers may be associated with reduced risk for Parkinson disease (PD).

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

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

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

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

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

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

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

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

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

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

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

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

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

257 locus in genome-wide association studies of Parkinson disease (PD).

258 connectivity of the nigrostriatal pathway in Parkinson disease (PD).

259 sfunction plays a role in the development of Parkinson disease (PD).

260 e the most important genetic risk factor for Parkinson disease (PD).

261 BA1 mutations are a frequent risk factor for Parkinson disease (PD).

262 eristics are potential prodromal markers for Parkinson disease (PD).

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

264 that immune system dysfunction has a role in Parkinson disease (PD); this evidence includes clinical

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

266 n isolated/idiopathic RBD (iRBD, n = 1,076), Parkinson disease (PD, n = 1,013), dementia with Lewy bo

267 cohort of patients with early MSA (n = 38), Parkinson disease (PD, n = 16), and dementia with Lewy b

268 ally followed 870 subjects with diagnoses of Parkinson disease (PD; n = 179), FTD (n = 179), Alzheime

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

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

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

272 0.5 points; 95% CI, -0.7 to 1.7; P = .41) or Parkinson Disease Questionnaire-39 summary index (0.007

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

274 ement Disorder Society [MDS]-revised Unified Parkinson Disease Rating Scale [UPDRS] [I-III] total sco

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

276 Baseline Unified Parkinson Disease Rating Scale part three scores (UPDRS-

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

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

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

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

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

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

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

284 h synaptic vesicle glycoprotein 2A (SV2A) in Parkinson disease subjects with mild bilateral disease (

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

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

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

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

289 For all patients with Parkinson disease, treatment is symptomatic, focused on

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

291 ain disorders such as autism, depression and Parkinson disease typically develop at certain stages of

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

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

294 In 129 patients with Parkinson disease, we retrospectively tested whether sle

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

296 ateral sclerosis and 3,769 incident cases of Parkinson disease were identified during the follow-up.

297 etrospectively investigated 21 patients with Parkinson disease with bilateral subthalamic deep brain

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

299 Fifty-five autopsy-confirmed LBD (Parkinson disease with dementia, n = 36; dementia with L

300 probable dementia with Lewy bodies (n = 1), Parkinson disease with mild cognitive impairment (n = 2)