ライフサイエンスコーパス: Parkinson's disease

1 to identify novel genes that cause familial Parkinson's disease.

2 evelopment of new therapeutic principles for Parkinson's disease.

3 ain DA nuclei are differentially affected in Parkinson's disease.

4 from three families with autosomal dominant Parkinson's disease.

5 development of impulse control disorders in Parkinson's disease.

6 ological degeneration of neural circuitry in Parkinson's disease.

7 trajectory and predictors for development of Parkinson's disease.

8 ogate immune biomarker of neuronal injury in Parkinson's disease.

9 lation is associated with the development of Parkinson's Disease.

10 ed in individuals suffering from early-onset Parkinson's disease.

11 ase in the pathogenesis of PRKN/PINK1-linked Parkinson's disease.

12 urological disorders, including dementia and Parkinson's disease.

13 RKN are the most common cause of early onset Parkinson's disease.

14 ) accumulation is a pathological hallmark of Parkinson's disease.

15 a role for inflammation in PRKN/PINK1-linked Parkinson's disease.

16 bilizes alpha-synuclein fibrils connected to Parkinson's disease.

17 RK2) are the most frequent cause of familial Parkinson's disease.

18 a wide range of synucleinopathies, including Parkinson's Disease.

19 of mitochondrial complex III dysfunction in Parkinson's disease.

20 different neurological disorders, including Parkinson's disease.

21 n vivo, consistent with a pathogenic role in Parkinson's disease.

22 evice for the treatment of motor symptoms of Parkinson's disease.

23 peutic option for managing motor symptoms of Parkinson's disease.

24 eimer's Disease, frontotemporal dementia, or Parkinson's Disease.

25 res the LTP-like plasticity in patients with Parkinson's disease.

26 ion neural circuit during the progression of Parkinson's disease.

27 suffered from early-onset l-DOPA-responsive Parkinson's disease.

28 chanisms of deep brain stimulation (DBS) for Parkinson's disease.

29 for neuron-mediated genetic diseases such as Parkinson's disease.

30 ls an unexpected role of oligodendrocytes in Parkinson's disease.

31 sms that explain the hypokinetic features of Parkinson's disease.

32 ound to cause an autosomal recessive form of Parkinson's disease.

33 mulation to treat cardinal motor features of Parkinson's disease.

34 n underlie conditions such as depression and Parkinson's disease.

35 imipramine, could be potential therapies for Parkinson's disease.

36 cal diseases, such as multiple sclerosis and Parkinson's disease.

37 nd therapy for off episodes in patients with Parkinson's disease.

38 deep brain stimulation on motor symptoms in Parkinson's disease.

39 involvement of the PSAP saposin D domain in Parkinson's disease.

40 cause of dopamine deficit in the striatum in Parkinson's disease.

41 modulating the LTP-like plasticity of M1 in Parkinson's disease.

42 ological disorders including Alzheimer's and Parkinson's diseases.

43 ronal function and health in Alzheimer's and Parkinson's diseases.

44 on, have also been linked to Alzheimer's and Parkinson's diseases.

45 s the most commonly mutated gene in familial Parkinson's disease(1) and is also linked to its idiopat

46 in a naturalistic fashion, 55 patients with Parkinson's disease (19 females, mean age 62, mean Hoehn

47 arkinsonism with dementia(1)-and early-onset Parkinson's disease(2).

48 mortem studies on two patients with advanced Parkinson's disease 8 and10 years following AAV2-neurtur

49 fusion-weighted imaging in 100 patients with Parkinson's disease (81 without hallucinations, 19 with

50 ary refers to 'Brain-first versus body-first Parkinson's disease: a multi-modal imaging case-control

51 These include Parkinson's disease, ADHD, schizophrenia, and mood disor

52 eature of neurodegenerative diseases such as Parkinson's disease, Alzheimer's disease and multiple sc

53 m human studies on microbiome alterations in Parkinson's disease, Alzheimer's disease, amyotrophic la

54 ns such as Alzheimer's disease (AD), stroke, Parkinson's disease, Amyotrophic lateral sclerosis (ALS)

55 The second cohort included 28 Parkinson's disease and 43 control samples.

56 reward, and pathological conditions such as Parkinson's disease and addiction.

57 f CNS diseases including multiple sclerosis, Parkinson's disease and amyotrophic lateral sclerosis re

58 10 (C10) were recently identified as causing Parkinson's disease and amyotrophic lateral sclerosis/fr

59 Visual hallucinations are common in Parkinson's disease and are associated with poorer progn

60 of neurodegenerative disorders, focusing on Parkinson's disease and cerebral ischemia.

61 rstood factor in human conditions related to Parkinson's disease and complex behaviors.SIGNIFICANCE S

62 ogical material for addressing diseases like Parkinson's Disease and Epilepsy.

63 f alpha-synuclein and tau linked to familial Parkinson's disease and frontotemporal dementia, respect

64 les, representing 40 patients) consisting of Parkinson's disease and healthy control samples from thr

65 such as in the case of Alzheimer's disease, Parkinson's disease and Huntington's disease.

66 In Parkinson's disease and its models, abnormal rates and p

67 e associated with Lewy body diseases such as Parkinson's disease and Lewy body dementia.

68 ations in alpha-synuclein are linked to both Parkinson's disease and Lewy body dementia; in particula

69 ynuclein aggregates that are associated with Parkinson's disease and multiple system atrophy correspo

70 ifferences between synucleinopathies such as Parkinson's disease and multiple system atrophy have bee

71 potential to discriminate between idiopathic Parkinson's disease and Parkinson's disease linked to he

72 verity in patients with early or progressing Parkinson's disease and patients with idiopathic rapid e

73 pamine neurons are especially susceptible to Parkinson's disease and prematurely degenerate in the co

74 brospinal fluid from patients diagnosed with Parkinson's disease and samples from patients with multi

75 nges that accompany visual hallucinations in Parkinson's disease and the organizational and gene expr

76 have been shown to contribute to the risk of Parkinson's disease, and currently 90 independent risk v

77 sociated with sporadic and familial forms of Parkinson's disease, and our finding suggests a genetic

78 human diseases, such as Alzheimer's disease, Parkinson's disease, and type 2 diabetes.

79 nerative diseases, including Alzheimer's and Parkinson's disease, are characterized by increased prot

80 By use of Parkinson's disease as a model condition, we show an int

81 have examined the modulation of the risk of Parkinson's disease as a result of the use of beta-adren

82 the subthalamic nucleus of 18 patients with Parkinson's disease as they executed cued upper and lowe

83 indings suggest that the increase in risk of Parkinson's disease associated with beta-adrenoceptor an

84 its interaction and colocalisation with the Parkinson's disease-associated E3 ubiquitin ligase Parki

85 The clinical spectrum of Parkinson's disease-associated gene carriers in this mai

86 genic/likely pathogenic variants in 23 known Parkinson's disease-associated genes occurred more frequ

87 likely pathogenic variants involved in known Parkinson's disease-associated genes.

88 sociation study and analysed the most recent Parkinson's disease-associated genetic risk score to det

89 Parkin has functions in the nucleus and that Parkinson's disease-associated Parkin mutants, ParkinR42

90 potential to influence the disease course of Parkinson's disease, at least in this subset of patients

91 The estimated risk of Parkinson's disease because of beta-adrenoceptor antagon

92 electrochemical sensors for the detection of Parkinson's disease biomarkers.

93 In Parkinson's disease, bradykinesia is characterized by sl

94 brain maladies such as Alzheimer's disease, Parkinson's disease, brain lymphomas, and other ailments

95 mography (PET) imaging that is used to image Parkinson's disease, brain tumors, and focal hyperinsuli

96 alamic nucleus is a symptomatic treatment of Parkinson's disease but benefits only to a minority of p

97 of dopaminergic neurons in familial forms of Parkinson's disease but the precise pathogenic mechanism

98 asets, totalling 217 165 individuals (22 757 Parkinson's disease cases, 13 431 Parkinson's disease pr

99 es and 180 355 controls), we identified 1691 Parkinson's disease cases, 81 Lewy body dementia cases,

100 identifies several novel protein changes in Parkinson's disease cerebrospinal fluid that may be expl

101 192, 33.85%) than in the autosomal-dominant Parkinson's disease cohort (10 of 242, 4.13%) and the sE

102 d more frequently in the autosomal-recessive Parkinson's disease cohort (65 of 192, 33.85%) than in t

103 Although Parkinson's disease commonly manifests with motor sympto

104 mimetics is associated with a lower rate of Parkinson's disease compared to the use of other oral an

105 LRRK2 associates with the susceptibility to Parkinson's disease, Crohn's disease, and mycobacteria i

106 In rodent models of Parkinson's disease, D1-mGlu5 nanocomplexes were strongl

107 nd aggregation of alpha-synuclein, including Parkinson's disease, dementia with Lewy bodies and multi

108 a-synuclein, a protein known to aggregate in Parkinson's disease, dementia with Lewy bodies, and mult

109 l role in neurodegenerative diseases such as Parkinson's disease, dementia with Lewy bodies, and mult

110 pid eye movement sleep behavioural disorder, Parkinson's disease, dementia with Lewy bodies, multiple

111 hat motor cortical high beta oscillations in Parkinson's disease demonstrate increased burst duration

112 he potential of IL6 as progression marker in Parkinson's disease due to PRKN/PINK1 mutations; (iii) i

113 f treatments for related conditions, such as Parkinson's disease, for the management of common sympto

114 erformance (AUC=0.86) in separating clinical Parkinson's disease from controls across populations.

115 patients in the Cambridgeshire Incidence of Parkinson's disease from General Practice to Neurologist

116 d multiple protein ratios that differentiate Parkinson's disease from healthy controls and validated

117 ynuclein and clusterin measurement predicted Parkinson's disease from other proteinopathies with AUC=

118 in PD.SIGNIFICANCE STATEMENT In persons with Parkinson's disease, gait dysfunction and the associated

119 nts appear to be in close proximity to known Parkinson's disease genes and lysosomal-related genes.

120 domain (rs4747203 and rs885828) in sporadic Parkinson's disease had significantly higher allele freq

121 fied a subnetwork of reduced connectivity in Parkinson's disease hallucinations.

122 gh our understanding of the genetic basis of Parkinson's disease has advanced considerably, much rema

123 eanwhile, studies of memory in patients with Parkinson's disease have focused on overall memory capac

124 Many patients with Parkinson's disease have potentially disabling off episo

125 ired, now that gene-targeting approaches for Parkinson's disease have reached the clinical trial stag

126 Patients with Parkinson's disease have reduced reward sensitivity rela

127 etic spectrum and clinical manifestations of Parkinson's disease in mainland China and expand the exi

128 we know relatively little of the genetics of Parkinson's disease in other populations.

129 The incidence of Parkinson's disease in patients diagnosed with diabetes

130 We compared the risk of Parkinson's disease in patients with diabetes exposed to

131 in one hemisphere improved motor features of Parkinson's disease in selected patients with asymmetric

132 Compared with the incidence of Parkinson's disease in the comparison group (10 per 10 0

133 Population data for risk of Parkinson's disease in users of the newer types of drugs

134 e wrist worn sensors in 35 participants with Parkinson's disease in-clinic and 25 participants monito

135 ssociation between the use of glitazones and Parkinson's disease [incidence rate ratio (IRR) 1.17; 95

136 Freezing of gait (FoG) in Parkinson's disease involves deficient anticipatory post

137 markers of disease progression in idiopathic Parkinson's disease (iPD).

138 hibitors and GLP-1 mimetics and the onset of Parkinson's disease (IRR 0.64; 95% CI 0.43-0.88; P < 0.0

139 Parkinson's disease is a complex neurodegenerative disor

140 Parkinson's disease is a genetically complex disorder.

141 Parkinson's disease is a synucleinopathy that is charact

142 Parkinson's disease is caused by a loss of dopaminergic

143 Parkinson's disease is characterized by the presence of

144 tric disorders, such as major depression and Parkinson's disease is enabled.

145 ained by reverse causation because prodromal Parkinson's disease is often associated with non-specifi

146 Parkinson's disease is the second most common neurodegen

147 gic projection neurons is a key pathology in Parkinson's disease, leading to abnormal function of bas

148 outcomes of the PD MED and Levodopa in Early Parkinson's Disease (LEAP) studies.

149 ons in neurodegenerative diseases, including Parkinson's disease, Lewy body dementia, and multiple sy

150 synuclein is a defining molecular feature of Parkinson's disease, Lewy body dementia, and multiple sy

151 proteolytic truncations of alphasyn occur in Parkinson's disease, Lewy body dementia, and multiple sy

152 k factor for neurologic disorders, such as a Parkinson's disease-like syndrome known as manganism.

153 e between idiopathic Parkinson's disease and Parkinson's disease linked to heterozygous PRKN/PINK1 mu

154 Previous studies on Parkinson's disease mechanisms have shown dysregulated e

155 Research on Parkinson's disease most often focuses on the ability of

156 tween LNB and dementia, Alzheimer's disease, Parkinson's disease, motor neuron disease, epilepsy, and

157 term risks of dementia, Alzheimer's disease, Parkinson's disease, motor neuron diseases, epilepsy, or

158 ased risks of dementia, Alzheimer's disease, Parkinson's disease, motor neuron diseases, or epilepsy.

159 trigger a series of human diseases, such as Parkinson's disease, multifactor disorder and Type-II di

160 xosomes as biomarkers across the spectrum of Parkinson's disease, multiple system atrophy and other p

161 tidase 4 (DPP4) inhibitors, with the risk of Parkinson's disease of users of any other oral glucose l

162 (n = 102) and from a comparative population (Parkinson's disease or healthy participants, n = 61).

163 ibrillar alpha-Syn polymorphs trigger either Parkinson's disease or multiple system atrophy hallmarks

164 y or corticobasal syndrome (AUC=88.47%), and Parkinson's disease or multiple systems atrophy (AUC=81.

165 tiple brain disorders and injuries, e.g., in Parkinson's disease or traumatic brain injury (TBI), and

166 r of neurons expressing dopamine could treat Parkinson's disease, or one affecting the number express

167 which include multiple system atrophy (MSA), Parkinson's disease, Parkinson's disease with dementia a

168 TREM2 differed between CSF biomarker-defined Parkinson's disease participant subgroups.

169 changes that occur during the progression of Parkinson's disease pathology will aid the development o

170 utilized to protect dopamine neurons against Parkinson's disease pathology.

171 We also demonstrate that medicated Parkinson's disease patients exert similar effort to gai

172 uring mutations in PRKN/PINK1 and idiopathic Parkinson's disease patients remain elusive.

173 Twenty-three Parkinson's disease patients with a history of impulse c

174 ghlight the importance of genetic testing in Parkinson's disease patients with age at onset < 40 year

175 Within this network, Parkinson's disease patients with hallucinations showed

176 ifferentiate, using a physiological measure, Parkinson's disease patients with impulse control disord

177 Specifically, the age at onset of Parkinson's disease patients with pathogenic/likely path

178 ss influence over other brain regions), than Parkinson's disease patients without hallucinations and

179 ia/macrophage derived exosomes in the CSF of Parkinson's disease patients, we confirmed the presence

180 ent brain and is in clinical trials to treat Parkinson's disease patients.

181 her levels of alpha-synuclein (alpha-syn) in Parkinson's disease patients.

182 such association was observed for idiopathic Parkinson's disease patients.

183 re, we demonstrate that Netrin1 reduction in Parkinson's disease (PD) activates MST1, which selective

184 Parkinson's disease (PD) affects millions of patients wo

185 Current therapeutic strategies for Parkinson's disease (PD) aim to delay progression or rep

186 regulated in the cerebellum of patients with Parkinson's disease (PD) and Essential Tremor (ET).

187 ed neurological movement disorders including Parkinson's Disease (PD) and Essential Tremor (ET).

188 An epidemiological connection exists between Parkinson's disease (PD) and melanoma.

189 repeat kinase 2 (LRRK2) is a common cause of Parkinson's disease (PD) and results in age-related dopa

190 Parkinson's disease (PD) and schizophrenia (SCZ) are her

191 tivity in the basal ganglia of patients with Parkinson's disease (PD) are associated with impaired mo

192 The concept of 'idiopathic' Parkinson's disease (PD) as a single entity has been cha

193 They can be precipitated in Parkinson's disease (PD) by dopamine replacement therapy

194 ely common mutation, associated with 1-3% of Parkinson's disease (PD) cases worldwide.

195 arameters in a large cohort of patients with Parkinson's disease (PD) compared to controls using a fu

196 se mutations cause, or increase the risk of, Parkinson's disease (PD) have been identified.

197 dividuals with freezing of gait (FoG) due to Parkinson's disease (PD) have small and long anticipator

198 In this review, we approach Parkinson's disease (PD) in the context of an evolutiona

199 Parkinson's disease (PD) is a common neurodegenerative d

200 Parkinson's disease (PD) is a multifactorial malady and

201 Parkinson's disease (PD) is a progressive neurodegenerat

202 We show that the common genetic risk for Parkinson's disease (PD) is associated with dopaminergic

203 Parkinson's disease (PD) is characterized by dopaminergi

204 transplantation can rescue motor defects in Parkinson's disease (PD) models, whether and how grafts

205 a dual pharmacological action of attenuating Parkinson's disease (PD) motor symptoms and development

206 factor (GDNF), and produce potent effects in Parkinson's disease (PD) mouse models.

207 nucleus deep brain stimulation (STN-DBS) in Parkinson's disease (PD) not only stimulates focal targe

208 Parkinson's disease (PD) pathogenesis may involve the ep

209 uman alpha-synuclein (alphaSyn) is linked to Parkinson's disease (PD) pathology.

210 nt (FMI) is progressively expressed in early Parkinson's Disease (PD) patients and is now known to be

211 utral lipids in the substantia nigra (SN) of Parkinson's disease (PD) patients and its relationship t

212 oses a significant health care challenge for Parkinson's disease (PD) patients.

213 rapeutic intervention.SIGNIFICANCE STATEMENT Parkinson's disease (PD) prevalence is projected to rise

214 ucleus (STN) deep brain stimulation (DBS) in Parkinson's disease (PD) remains unclear.

215 vement in neurodegenerative diseases such as Parkinson's disease (PD) remains unclear.

216 xposure to lipid-lowering drugs might affect Parkinson's disease (PD) risk.

217 The genetics and pathophysiology of Parkinson's disease (PD) strongly implicate mitochondria

218 esent study profiled two EMVs from different Parkinson's disease (PD) tissue sources: (a) neural prog

219 n the brains of Alzheimer's disease (AD) and Parkinson's disease (PD) with dementia (PDD) patients, w

220 DDRs are upregulated in Alzheimer's and Parkinson's disease (PD), and DDRs knockdown reduces neu

221 mpairment) on the phenotype of LRRK2 and GBA Parkinson's disease (PD), and on the prevalence of prodr

222 ion in neurodegenerative diseases, including Parkinson's disease (PD), and optimal modulation of thes

223 ta activity is linked to symptom severity in Parkinson's disease (PD), but few studies have character

224 n brain and drives symptom lateralization in Parkinson's disease (PD), but its molecular determinants

225 m is one of most common nonmotor symptoms in Parkinson's disease (PD), but the molecular role of the

226 ting neurodegenerative conditions, including Parkinson's disease (PD), dementia with Lewy bodies (DLB

227 In Parkinson's disease (PD), gamma oscillatory activity in

228 osomes predates the clinical presentation of Parkinson's disease (PD), offering a means of developing

229 We also analyzed six cases of idiopathic Parkinson's disease (PD), one case of familial PD, and s

230 In Parkinson's disease (PD), pathologically high levels of

231 l sclerosis (ALS), Alzheimer's disease (AD), Parkinson's disease (PD), vascular dementia (VD), senile

232 hibitors that specifically target seeding of Parkinson's disease (PD)-associated alpha-synuclein (alp

233 The Parkinson's disease (PD)-associated gene leucine-rich re

234 The PPIase CypA colocalizes with the Parkinson's disease (PD)-associated protein alpha-synucl

235 aired 5'-phosphatase activity, also leads to Parkinson's disease (PD)-like pathologies in mice.

236 Here, we show that the Parkinson's disease (PD)-related kinase LRRK2 is activat

237 avioural disorder (RBD) are risk factors for Parkinson's disease (PD).

238 ccepted as a key step in the pathogenesis of Parkinson's disease (PD).

239 m involvement precedes the motor features of Parkinson's disease (PD).

240 n enigmatic enzyme and a relevant target for Parkinson's disease (PD).

241 ociated with autosomal recessive early-onset Parkinson's disease (PD).

242 s in Parkin are a major cause of early-onset Parkinson's disease (PD).

243 ted with dementia with Lewy bodies (DLB) and Parkinson's disease (PD).

244 effective therapy for the motor symptoms of Parkinson's disease (PD).

245 um of neurodegenerative disorders, including Parkinson's disease (PD).

246 stress disorder (PTSD) are risk factors for Parkinson's disease (PD).

247 many neurodegenerative disorders, including Parkinson's disease (PD).

248 nase 2 (LRRK2) is a common cause of familial Parkinson's disease (PD).

249 e of late-onset, autosomal-dominant familial Parkinson's disease (PD).

250 e associated with elevated long-term risk of Parkinson's disease (PD).

251 can self-aggregate and plays a major role in Parkinson's disease (PD).

252 energic signaling are ubiquitous features of Parkinson's disease (PD).

253 been identified as a common risk factor for Parkinson's disease (PD).

254 iation between mitochondrial dysfunction and Parkinson's disease (PD).

255 a treatment for non-motor symptoms (NMS) in Parkinson's disease (PD).

256 a surgical therapy with class 1 evidence for Parkinson's disease (PD).

257 implicated in the neurodegenerative disorder Parkinson's disease (PD); however, it is unclear how mit

258 SNCA has been implicated in the etiology of Parkinson's disease (PD); however, the normal function o

259 ral sclerosis (ALS), multiple sclerosis, and Parkinson's disease, peripheral nervous system (PNS) dis

260 alpha-synuclein remains stably elevated with Parkinson's disease progression.

261 Parkinson's disease protein 7 (PARK7/DJ-1) was successfu

262 ls (22 757 Parkinson's disease cases, 13 431 Parkinson's disease proxy cases, 622 Lewy body dementia

263 d Yahr scale, Montreal Cognitive Assessment, Parkinson's Disease Questionnaire-39 and PD subtype asse

264 ose in the Movement Disorder Society Unified Parkinson's Disease Rating Scale (MDS-UPDRS) part 3 (mot

265 using the Movement Disorders Society Unified Parkinson's Disease Rating Scale (MDS-UPDRS).

266 ion of the Movement Disorder Society-Unified Parkinson's Disease Rating Scale (MDS-UPDRS-III), and el

267 es on the Movement Disorders Society Unified Parkinson's Disease Rating Scale (total score 4.6 [SD 4.

268 he primary outcome was change in the Unified Parkinson's Disease Rating Scale (UPDRS) parts I to III

269 D scored significantly higher on the Unified Parkinson's Disease Rating Scale motor subscale than oth

270 n and the Movement Disorders Society Unified Parkinson's Disease Rating Scale part 3 (UPDRS-III).

271 d Montreal Cognitive Assessment, and Unified Parkinson's Disease Rating Scale score was obtained in p

272 A gene associated with Parkinson's disease regulates mitochondrial homeostasis,

273 ture in patients with YOPD who have no known Parkinson's disease-related mutations, suggesting that t

274 ume of the substantia nigra in patients with Parkinson's disease relative to the controls was best fi

275 f heterozygous mutations in PRKN or PINK1 as Parkinson's disease risk factor.

276 s disease would be small compared with other Parkinson's disease risk factors and would be similar to

277 nverted haplotype of the MAPT (encoding tau) Parkinson's disease risk locus, identifying putative ect

278 alleles that have been identified, although Parkinson's disease risk variants appear to be in close

279 isease, and whether these overlap with known Parkinson's disease risk variants.

280 ll-free mtDNA levels may serve as markers of Parkinson's disease state and progression, respectively.

281 motor symptoms, a majority of patients with Parkinson's disease subsequently develop cognitive impai

282 is, mild cognitive impairment, dementia, and Parkinson's disease, supporting the relevance of brainst

283 of alpha-synuclein, a protein implicated in Parkinson's disease that predominately nucleates on memb

284 The incidence of Parkinson's disease was 8 per 10 000 person-years in 21

285 Notably, Parkinson's disease was genetically associated not only

286 bumin-expressing neurons in a mouse model of Parkinson's disease, we discovered evidence for an upreg

287 tion of microglial activation with advancing Parkinson's disease, we investigated whether CSF and/or

288 eficits of dopamine-depleted mouse models of Parkinson's disease, where cell type-specific optogeneti

289 st genetic and environmental risk factors of Parkinson's disease, whereas loss of ATP13A2 compromises

290 PRKN/PINK1 mutations compared to idiopathic Parkinson's disease, which is in line with previous find

291 agonist propranolol and an increased risk of Parkinson's disease, while the chronic use of the beta-a

292 Patients with Parkinson's disease who had 2 h or more of off time per

293 2:1 ratio, patients with markedly asymmetric Parkinson's disease who had motor signs not fully contro

294 ity (256 channels) EEG from 31 patients with Parkinson's disease who underwent deep brain stimulation

295 by a dose-dependent decrease in the risk of Parkinson's disease with chronic beta-adrenoceptor agoni

296 e system atrophy (MSA), Parkinson's disease, Parkinson's disease with dementia and dementia with Lewy

297 ly normal elderly subjects, 45 patients with Parkinson's disease with no cognitive impairment, 86 wit

298 n 22 and 75 years, a diagnosis of idiopathic Parkinson's disease with over 5 years of motor symptoms,

299 ignificant enrichment of the heritability of Parkinson's disease within the substantia nigra module.

300 beta-adrenoceptor antagonists on the risk of Parkinson's disease would be small compared with other P