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1 netic Resonance Imaging in ten patients with Parkinson's disease.
2  neurons is a promising approach to treating Parkinson's disease.
3  in the cytoplasm of degenerating neurons in Parkinson's disease.
4 k between synaptic endocytic dysfunction and Parkinson's disease.
5  hypotheses for dopaminergic neuron death in Parkinson's disease.
6  as observed in age-related diseases such as Parkinson's disease.
7 gical diseases, including drug addiction and Parkinson's disease.
8  international longitudinal study of de novo Parkinson's disease.
9 d in mitochondrial homeostasis and linked to Parkinson's disease.
10 e diseases including Alzheimer's disease and Parkinson's disease.
11 / hyperactivity disorder, schizophrenia, and Parkinson's disease.
12 2AR-selective compounds for the treatment of Parkinson's disease.
13 nitive health or impairment in patients with Parkinson's disease.
14 of glioblastoma, traumatic brain injury, and Parkinson's disease.
15 e diseases including Alzheimer's disease and Parkinson's disease.
16 ein, a protein forming amyloid aggregates in Parkinson's disease.
17 fy novel predictors for motor progression in Parkinson's disease.
18 ctional protein in a patient with late onset Parkinson's disease.
19  models in the design of treatment trials in Parkinson's disease.
20 er disease, are also potent risk factors for Parkinson's disease.
21 vicious cycle scenario faced by microglia in Parkinson's disease.
22 tility observed in patients with early-stage Parkinson's disease.
23 oprotective effects in preclinical models of Parkinson's disease.
24  the brain in patients with Huntington's and Parkinson's disease.
25 neurodegenerative disorder associated to the Parkinson's disease.
26 e disease phenotype in a C. elegans model of Parkinson's disease.
27 ceptor that is a target for the treatment of Parkinson's disease.
28 tibility, and the underlying neurobiology of Parkinson's disease.
29 gic innervation preceding the motor onset of Parkinson's disease.
30 t DOPA decarboxylase (DDC), a key protein in Parkinson's disease.
31 GF-beta signaling as a potential therapy for Parkinson's disease.
32 y increased risk for melanoma in people with Parkinson's disease.
33 rease in neurodegenerative disorders such as Parkinson's disease.
34 represent the most prevalent risk factor for Parkinson's disease.
35 brain communication, such as Alzheimer's and Parkinson's diseases.
36 generative disorders such as Alzheimer's and Parkinson's diseases.
37 erative disorders, including Alzheimer's and Parkinson's diseases.
38 cantly reduced in Alzheimer's, Huntington's, Parkinson's diseases.
39 ocerebrosidase receptor, impacts Gaucher and Parkinson's diseases.
40 orders including stroke, and Alzheimer's and Parkinson's diseases.
41                                           In Parkinson's disease, a disease-specific physiomarker was
42 he time of clinical diagnosis, patients with Parkinson's disease already have a wide range of motor a
43 everal brain disorders, including addiction, Parkinson's disease, Alzheimer's disease and schizophren
44 16 rest tremor recordings in tremor-dominant Parkinson's disease and 20 postural tremor recordings in
45 s in free water in 103 de novo patients with Parkinson's disease and 49 controls; (ii) 2- and 4-year
46  insights into other behavioural symptoms in Parkinson's disease and addictions in the general popula
47  findings with those in people with sporadic Parkinson's disease and age-matched healthy controls.
48 13-35 Hz) is commonly found in patients with Parkinson's disease and can be suppressed by dopaminergi
49 nuclein family has long been associated with Parkinson's disease and dementia.
50 ent cohort comprising a further 55 tremulous Parkinson's disease and essential tremor recordings.
51                                              Parkinson's disease and experimentally induced hemiparki
52 ar and clinical variables from patients with Parkinson's disease and healthy controls to construct an
53 apeutic interventions to treat patients with Parkinson's disease and impulse control disorders have s
54                             In patients with Parkinson's disease and impulse control disorders, impai
55  misfolding and aggregation is a hallmark in Parkinson's disease and in several other neurodegenerati
56  are similar in LRRK2 mutation carriers with Parkinson's disease and individuals with sporadic Parkin
57 ion in LRRK2 mutation carriers with manifest Parkinson's disease and individuals with sporadic Parkin
58 rhabditis elegans) and the major symptoms of Parkinson's disease and primary progressive freezing gai
59 ew insight into mitochondrial pathologies in Parkinson's disease and provide new prospects for target
60 ion and neurotoxicity to the pathogenesis of Parkinson's disease and related alpha-synucleinopathies.
61 ld be a means of therapeutic intervention in Parkinson's disease and related conditions.
62 n have been linked to neuronal impairment in Parkinson's disease and related neurodegenerative disord
63 ent of PARK2, a gene intensively reported in Parkinson's disease and schizophrenia research.
64  been reported to be associated with autism, Parkinson's disease and schizophrenia, respectively.
65 icates that the CNR2 gene is associated with Parkinson's disease and substance use disorders.
66 associated with a probable decreased risk of Parkinson's disease and type-2 diabetes and an increased
67 e pathways of Alzheimer's, Huntington's, and Parkinson's diseases and has been identified as a potent
68  incident cases of dementia, 31 577 cases of Parkinson's disease, and 9247 cases of multiple sclerosi
69 mutation carriers, individuals with sporadic Parkinson's disease, and age-matched healthy controls se
70 st Parkinson's disease, people with sporadic Parkinson's disease, and age-matched healthy controls, a
71 ilarities between dementia with Lewy bodies, Parkinson's disease, and Alzheimer's disease.
72  substantia nigra as a progression marker in Parkinson's disease, and describe the pattern of progres
73 ents a major new avenue for investigation in Parkinson's disease, and effects on everyday symptoms sh
74 rative diseases such as Alzheimer's disease, Parkinson's disease, and Huntington's disease.
75 er's disease, amyotrophic lateral sclerosis, Parkinson's disease, and Huntington's disease.
76 , epilepsy, autism, Alzheimer's disease, and Parkinson's disease, and is considered a potential targe
77 phaS) is the primary protein associated with Parkinson's disease, and it undergoes aggregation from i
78              Incident diagnoses of dementia, Parkinson's disease, and multiple sclerosis were ascerta
79 relationship with the incidence of dementia, Parkinson's disease, and multiple sclerosis.
80                   Dementia with Lewy bodies, Parkinson's disease, and Multiple System Atrophy are age
81 ation carriers, 13 individuals with sporadic Parkinson's disease, and nine healthy controls.
82 acular degeneration, traumatic brain injury, Parkinson's disease, and other neurodegenerations.
83 ression, schizophrenia, Alzheimer's disease, Parkinson's disease, and pain, provides convincing evide
84 mpared with controls, individuals with LRRK2 Parkinson's disease, and people with sporadic Parkinson'
85 models for amyotrophic lateral sclerosis and Parkinson's disease, and show a partial rescue of the Pa
86  which is vulnerable to neurodegeneration in Parkinson's disease, and the calbindin-positive dorsal t
87 er's disease, amyotrophic lateral sclerosis, Parkinson's disease, and the prototypic neuroinflammator
88 nson's disease and individuals with sporadic Parkinson's disease, and whether LRRK2 mutation carriers
89 ncers; cardiovascular disease and mortality; Parkinson's disease; and type-2 diabetes.
90 tions used in the treatment of patients with Parkinson's disease are associated with motor and non-mo
91                       Progression markers of Parkinson's disease are crucial for successful therapeut
92                Stem cell-based therapies for Parkinson's disease are moving into a new and exciting e
93 ified, its roles in other disorders, such as Parkinson's disease, are starting to emerge, and A2AR an
94 nerative diseases, including Alzheimer's and Parkinson's disease, are thought to spread to increasing
95 tients were aged 25-75 years, had idiopathic Parkinson's disease as measured by Queen Square Brain Ba
96 i-site cohorts, and increased over 1 year in Parkinson's disease but not in controls at a single site
97    The latter is not constantly increased in Parkinson's disease, but comes in bursts of different du
98 nson's disease and individuals with sporadic Parkinson's disease, but LRRK2 mutation carriers without
99 tations are the most common genetic cause of Parkinson's disease, but LRRK2's normal physiological ro
100 s approach may enable clinical therapies for Parkinson's disease by delivery of genes rather than cel
101 esigned to generate a more faithful model of Parkinson's disease by injecting human alpha-syn fibril
102  Paper: Prying into the Prion Hypothesis for Parkinson's Disease, by Patrik Brundin and Ronald Melki.
103 standing of this step in the pathogenesis of Parkinson's disease can facilitate the development of di
104                                  People with Parkinson's disease can show premotor neurochemical chan
105 seases (i.e., Alzheimer's, Huntington's, and Parkinson's diseases), carcinogenesis, stroke, intracere
106                                              Parkinson's disease cases also increasingly reported anx
107 raging whole exome sequencing data from 1156 Parkinson's disease cases and 1679 control subjects.
108                         In the past 5 years, Parkinson's disease cases developed additional motor fea
109 ears before diagnosis onwards, prediagnostic Parkinson's disease cases more commonly had problems in
110 e responsible for the majority of hereditary Parkinson's disease cases.
111 arkinson's patients selected from the Oxford Parkinson's Disease Centre Discovery Cohort and, after q
112 ompensatory processes.SIGNIFICANCE STATEMENT Parkinson's disease classically first becomes manifest i
113  55-85 years (about 2.2 million; dementia or Parkinson's disease cohort) who resided in Ontario, Cana
114 e posterior substantia nigra was elevated in Parkinson's disease compared to controls across single-
115 hway.SIGNIFICANCE STATEMENT Individuals with Parkinson's disease dementia often suffer a characterist
116  the treatment of synucleinopathies, such as Parkinson's disease, dementia with Lewy bodies, and mult
117 non-motor features in the 23 years preceding Parkinson's disease diagnosis by performing a nested cas
118                             In patients with Parkinson's disease, elevations in beta activity (13-35
119 sing data from nine cohorts of patients with Parkinson's disease from North America and Europe assess
120                  Neurotoxins associated with Parkinson's disease fully engages ER-p38 MAPK-CMA pathwa
121     BACKGROUND & AIMS: In most patients with Parkinson's disease, gastrointestinal (GI) dysfunctions,
122 ine LRRK2 mutation carriers without manifest Parkinson's disease had significantly elevated serotonin
123                                     Sporadic Parkinson's disease has been proposed to develop after i
124   Loss of dopaminergic (DA) neurons leads to Parkinson's disease; however, the mechanism(s) for the v
125 n free water in a subset of 46 patients with Parkinson's disease imaged at baseline, 12, 24, and 48 m
126 n conclusion, in patients with prediagnostic Parkinson's disease, impairments in instrumental daily a
127 eveloped clinically defined synucleinopathy (Parkinson's disease in 11, dementia with Lewy bodies in
128 might model aspects of the neuropathology of Parkinson's disease in mouse, we targeted RGMa to adult
129 h to study basal ganglia pathologies such as Parkinson's disease in silico.
130 ted approach to study BG pathologies such as Parkinson's disease in silico.
131 Here we describe an alternative strategy for Parkinson's disease in which dopamine neurons are genera
132  contribute to clinical differences in LRRK2 Parkinson's disease, including the emergence of non-moto
133                       Neurotoxins that mimic Parkinson's disease increased Cav1.3 function, decreased
134                                           In Parkinson's disease, intracellular alpha-synuclein inclu
135             Deep brain stimulation (DBS) for Parkinson's disease is a highly effective treatment in c
136                                              Parkinson's disease is associated with an increased inci
137 gy-independent manner.SIGNIFICANCE STATEMENT Parkinson's disease is characterized by progressive moto
138 he future.Dual Perspectives Companion Paper: Parkinson's Disease Is Not Simply a Prion Disorder, by D
139  to be phosphorylated in the presence of the Parkinson's disease kinase PINK1 but the downstream sign
140  non-invasively alleviated symptoms in mouse Parkinson's disease models.
141 tablished and identified novel predictors of Parkinson's disease motor progression.
142  the most common neurosurgical treatment for Parkinson's disease motor symptoms.
143 elated diseases such as Alzheimer's disease, Parkinson's disease, multiple sclerosis and cardiovascul
144        LRRK2 mutation carriers with manifest Parkinson's disease (n=15) had reduced striatal dopamine
145     LRRK2 mutation carriers without manifest Parkinson's disease (n=25) had greater (18)F-FDOPA uptak
146                          In a mouse model of Parkinson's disease, NeAL218 alone reprograms adult stri
147 th amounts seen in individuals with sporadic Parkinson's disease of similar duration.
148 shopping occur in about 17% of patients with Parkinson's disease on dopamine agonists.
149                No association was found with Parkinson's disease or multiple sclerosis.
150 a higher incidence of dementia, but not with Parkinson's disease or multiple sclerosis.
151 -9)), cognitive decline (P=5.3 x 10(-4)) and Parkinson's disease (P=8.6 x 10(-3)).
152 arkinson's disease, and people with sporadic Parkinson's disease, p<0.0001), striatum (compared with
153 d with LRRK2 mutation carriers with manifest Parkinson's disease, p=0.01), after adjustment for age.
154 striatum (compared with people with sporadic Parkinson's disease, p=0.02), and brainstem (compared wi
155 ce the importance of lysosomal mechanisms in Parkinson's disease pathogenesis.
156 ior of alpha-synuclein is a key component in Parkinson's disease pathogenesis.
157 nuclein (alpha-SYN) is a central molecule in Parkinson's disease pathogenesis.
158               Following genetic screening of Parkinson's disease patients and healthy controls, we al
159                                              Parkinson's disease patients demonstrated an altered pat
160 N) activity and electroencephalography in 11 Parkinson's disease patients during a perceptual decisio
161 corded from the subthalamic nucleus of eight Parkinson's disease patients during temporary lead exter
162 howed non-motor symptoms experienced by many Parkinson's disease patients including impaired cognitiv
163                                     Eighteen Parkinson's disease patients learned through feedback ON
164  from deep brain stimulation electrodes in 9 Parkinson's disease patients.
165  appearance of dyskinesia in the majority of Parkinson's disease patients.
166 ively correlated with clinical impairment in Parkinson's disease patients.
167            Studies suggest a greater risk of Parkinson's disease (PD) after traumatic brain injury (T
168 lphaS) forms round cytoplasmic inclusions in Parkinson's disease (PD) and dementia with Lewy bodies (
169 rative conditions (Alzheimer's disease (AD), Parkinson's disease (PD) and Huntington's disease (HD),
170   Neuroendocrine abnormalities are common in Parkinson's disease (PD) and include disruption of melat
171 alpha-syn) toxicity, a protein implicated in Parkinson's Disease (PD) and other neurodegenerative dis
172 (GBA) confer a heightened risk of developing Parkinson's disease (PD) and other synucleinopathies, re
173 ative disorders and is a hallmark feature of Parkinson's disease (PD) and PD-related diseases.
174                        The motor symptoms of Parkinson's disease (PD) are linked to abnormally correl
175 ) is increasingly used in mid- to late-stage Parkinson's disease (PD) but with an incomplete knowledg
176 computational model for beta oscillations in Parkinson's disease (PD) can also account for complex pa
177 ohort of, at baseline, patients with de novo Parkinson's disease (PD) compared with healthy controls
178 re to PM air pollution is related to risk of Parkinson's disease (PD) in the Health Professionals Fol
179                                              Parkinson's disease (PD) is a chronic and progressive ne
180                                              Parkinson's disease (PD) is a circuit-level disorder wit
181                                              Parkinson's disease (PD) is a neurodegenerative disease
182 patients and carriers.SIGNIFICANCE STATEMENT Parkinson's disease (PD) is a prevalent neurodegenerativ
183                                              Parkinson's disease (PD) is associated with increased ir
184                                              Parkinson's disease (PD) is associated with the formatio
185                                              Parkinson's disease (PD) is characterized by a progressi
186                                              Parkinson's disease (PD) is characterized by slow, progr
187                                              Parkinson's disease (PD) is defined by the loss of dopam
188                                              Parkinson's disease (PD) is highly comorbid for a spectr
189                    While the pathogenesis of Parkinson's disease (PD) is incompletely understood, mit
190                                              Parkinson's disease (PD) is one of the most common neuro
191                                              Parkinson's disease (PD) is the most common neurodegener
192                          A major hallmark of Parkinson's disease (PD) is the presence of Lewy bodies
193                             Individuals with Parkinson's disease (PD) often suffer from comorbid depr
194 a-Synuclein (alphaS) has a prominent role in Parkinson's disease (PD) pathology.
195                                              Parkinson's disease (PD) patients accumulate misfolded a
196 s of purified iPSC-derived DaNs derived from Parkinson's disease (PD) patients carrying LRRK2 G2019S
197                                              Parkinson's disease (PD) patients experience loss of nor
198  of cellular dysfunctions which may underlie Parkinson's disease (PD) progression.
199                                              Parkinson's Disease (PD) psychosis refers to the spectru
200            Using a transgenic mouse model of Parkinson's disease (PD) that expresses GFP-ASYN driven
201 paminergic (mDA) neurons from stem cells for Parkinson's Disease (PD) therapy; however, production of
202 Here, we tested the ability of patients with Parkinson's disease (PD) to maximize monetary rewards an
203  of 'awake' deep brain stimulation (DBS) for Parkinson's disease (PD) under local or general anaesthe
204 reductions of cerebral glucose metabolism in Parkinson's disease (PD) with 18F-fluorodeoxyglucose (FD
205         Retinal degeneration is prominent in Parkinson's disease (PD), a neuromotor disorder associat
206                          PINK1 is mutated in Parkinson's disease (PD), and mutations cause mitochondr
207 lay a primary role in the pathophysiology of Parkinson's disease (PD), and small molecules that count
208 ght as a novel target for both addiction and Parkinson's disease (PD), as well as other emerging dise
209 PARK7 are a rare cause of familial recessive Parkinson's disease (PD), but growing evidence suggests
210 ntia nigra dopaminergic neurodegeneration in Parkinson's disease (PD), but how these pathways are lin
211 function and dementia are common features of Parkinson's disease (PD), causing significant disability
212 everal neurodegenerative diseases, including Parkinson's disease (PD), creating a critical need to id
213  disorders such as Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease (HD), and
214 of toxic aggregates in neurons vulnerable in Parkinson's disease (PD), including dopaminergic neurons
215                   To understand the cause of Parkinson's disease (PD), it is important to determine t
216 cated in neurodegenerative disorders such as Parkinson's disease (PD), it is important to examine how
217 del is the most widely used animal model for Parkinson's disease (PD), it is known that nigrostriatal
218        By applying PRISM to a yeast model of Parkinson's disease (PD), we identified guide RNAs (gRNA
219 phaSyn) is the major gene linked to sporadic Parkinson's disease (PD), whereas the G209A (p.A53T) alp
220 kinase 2 (LRRK2) and alpha-synuclein lead to Parkinson's disease (PD).
221 ve symptomatic therapy for motor deficits in Parkinson's disease (PD).
222 a (SN) to neurodegenerative stressors causes Parkinson's disease (PD).
223 oxicity are important etiological factors in Parkinson's disease (PD).
224 bute to the progression of neuropathology in Parkinson's disease (PD).
225 ful in identifying genes that cause familial Parkinson's disease (PD).
226 -synuclein as a possibly causative factor in Parkinson's disease (PD).
227 tions in LRRK2 are a common cause of genetic Parkinson's disease (PD).
228 ognitive impairment (MCI) is common in early Parkinson's disease (PD).
229 ociated with autosomal recessive early-onset Parkinson's disease (PD).
230 neurone disease) (sporadic and familial) and Parkinson's Disease (PD).
231 that contribute to falls among subjects with Parkinson's disease (PD).
232 compacta (SNpc) preferentially degenerate in Parkinson's disease (PD).
233 suggests that synapses are affected first in Parkinson's disease (PD).
234 ions is the defining pathological process in Parkinson's disease (PD).
235  have, to date, identified >24 risk loci for Parkinson's disease (PD).
236 or neurosurgical treatment of motor signs of Parkinson's disease (PD).
237  are the most common genetic risk factor for Parkinson's disease (PD).
238 ha-SYN) is a major pathologic contributor to Parkinson's disease (PD).
239 ssociated with increased risk for developing Parkinson's disease (PD).
240 in (alpha-syn) aggregation is a key event in Parkinson's disease (PD).
241 e of serotonergic pathology in patients with Parkinson's disease (PD).
242 ) is an emerging target for the treatment of Parkinson's disease (PD).
243  pars compacta (SNc) dopaminergic neurons in Parkinson's disease (PD).
244 reams and is a potential prodromal marker of Parkinson's disease (PD).
245 to the pathology of complex diseases such as Parkinson's Disease (PD).
246 ith an increased risk for the development of Parkinson's disease (PD).
247 ssociated with risk of familial and sporadic Parkinson's disease (PD).
248 itochondrial dysfunction and pathogenesis of Parkinson's disease (PD).
249 ted in monogenic recessive familial cases of Parkinson's disease (PD).
250 ), Creutzfeldt-Jakob disease (CJD, n = 239), Parkinson's disease (PD, n = 39), dementia with Lewy bod
251 2 mutation carriers with or without manifest Parkinson's disease, people with sporadic Parkinson's di
252 ions of Parkin cause some monogenic forms of Parkinson's disease, possibly through its role in mitoch
253                                              Parkinson's disease predisposing LRRK2 kinase phosphoryl
254 rexpression of mutant alpha-synuclein causes Parkinson's disease, presumably by driving neurodegenera
255 or cell type in the brain, yet their role in Parkinson's disease progression remains elusive.
256 ce in the Movement Disorders Society Unified Parkinson's Disease Rating Scale (MDS-UPDRS) motor subsc
257  using the Movement Disorder Society Unified Parkinson's Disease Rating Scale (MDS-UPDRS) Part I scor
258 luding the Movement Disorder Society Unified Parkinson's Disease Rating Scale (MDS-UPDRS) part III, o
259 s from the Movement Disorder Society-Unified Parkinson's Disease Rating Scale (MDS-UPDRS) parts II an
260 e were no significant differences in Unified Parkinson's Disease Rating Scale (UPDRS) Section II scor
261 Scale, and Movement Disorder Society Unified Parkinson's Disease Rating Scale motor scores; 0.76, 0.6
262 rior, and whole SNpc correlated with Unified Parkinson's Disease Rating Scale scores (r(2) = 0.25, 0.
263  analyses, and correlations with the Unified Parkinson's Disease Rating Scale scores were tested.
264  change in PD clinical scale scores (Unified Parkinson's Disease Rating Scale) and DAT imaging during
265  symptoms (Movement Disorder Society Unified Parkinson's Disease Rating Scale, MDS-UPDRS III), fitnes
266                            390 patients with Parkinson's disease recruited between July 1, 2010, and
267 ses, we hypothesized that of the three major Parkinson's disease-related proteins-alpha-synuclein, LR
268 nvolved in amyotrophic lateral sclerosis and Parkinson's disease, respectively, using the small nine
269 e disorder gene variants in association with Parkinson's disease risk.
270 s well as neuropsychiatric disorders such as Parkinson's disease, schizophrenia, mood disorders, and
271                                           In Parkinson's disease, several studies have shown the feas
272 but LRRK2 mutation carriers without manifest Parkinson's disease show increased serotonin transporter
273 ine vs 7.33 [3.52] after dim-red LT) and the Parkinson's Disease Sleep Scale (97.24 [22.49] at baseli
274 e sex, and increased age, as well as a novel Parkinson's disease-specific epistatic interaction, all
275 milies with dominant inheritance patterns of Parkinson's disease, suggesting that it might confer a s
276                             In patients with Parkinson's disease, the grafted tissue was characterize
277           INTERPRETATION: In newly diagnosed Parkinson's disease, the occurrence of cognitive impairm
278 ction mutations of PINK1 lead to early onset Parkinson's disease, there has been growing interest in
279 sorders and the neuropsychiatric symptoms of Parkinson's disease, these findings have clinical implic
280 ate with graft outcome in an animal model of Parkinson's disease through gene expression analysis of
281 lly relevant neuroendocrine abnormalities in Parkinson's disease to highlight their role in overall p
282 ere loss, as seen in Alzheimer's disease and Parkinson's disease, to relatively little loss, as seen
283 abetes mellitus, a-synuclein associated with Parkinson's disease, transthyretin V30M mutant associate
284 .05 gave good classification performance for Parkinson's disease tremor and essential tremor, in both
285  neurosurgery for movement disorders such as Parkinson's disease, tremor, and dystonia involves the p
286  of dopaminergic neurons in a mouse model of Parkinson's disease using 1-methyl-4-phenyl-1,2,3,6-tetr
287 ubjects and a group of elderly subjects with Parkinson's disease using an event-related functional MR
288 tivity on non-motor symptoms associated with Parkinson's disease using conditional knockout (cKO) mic
289 rt was followed-up for the onset of clinical Parkinson's disease using several overlapping modalities
290 ebo-controlled trial, patients with moderate Parkinson's disease were randomly assigned (1:1) to rece
291 nts suffering from dopamine depletion due to Parkinson's disease were selectively impaired in reward
292  gait and posture, phenotypes reminiscent of Parkinson's disease, were evident when the mutation was
293 egenerative diseases such as Alzheimer's and Parkinson's disease where optic nerve involvement has, u
294 ra is a valid, progression imaging marker of Parkinson's disease, which may be used in clinical trial
295 cally defined off-medication motor scores in Parkinson's disease, which were sustained beyond the per
296 so be seen in patients with Huntington's and Parkinson's disease who had received foetal neural allog
297  and striatal binding ratio in a subgroup of Parkinson's disease who had undergone both diffusion and
298                           3200 patients with Parkinson's disease who were longitudinally assessed wit
299 enetic studies have shown the association of Parkinson's disease with alleles of the major histocompa
300 ese responses may explain the association of Parkinson's disease with specific major histocompatibili
301 r binding than did individuals with sporadic Parkinson's disease, with (18)F-FDOPA uptake comparable

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