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1 underscoring a pathophysiology distinct from idiopathic Parkinson's disease.
2 emerging earlier and more frequently than in idiopathic Parkinson's disease.
3 s, 25 healthy controls, and 25 patients with idiopathic Parkinson's disease.
4 PINK1-mitophagy is a contributing factor to idiopathic Parkinson's disease.
5 ciated with GBA mutations, and modestly with idiopathic Parkinson's disease.
6 2) are the most common cause of familial and idiopathic Parkinson's disease.
7 ld improve postural control in patients with idiopathic Parkinson's disease.
8 nsation for dopamine loss in experimental or idiopathic Parkinson's disease.
9 ofile similar to that previously reported in idiopathic Parkinson's disease.
10 t the causative role of paraquat exposure in idiopathic Parkinson's disease.
11 pamine neurons is characteristic of advanced idiopathic Parkinson's disease.
12 ) has an increasing role in the treatment of idiopathic Parkinson's disease.
13 tation, and had typical clinical findings of idiopathic Parkinson's disease.
14 veries and to discuss their relationships to idiopathic Parkinson's disease.
15 tern of nigrostriatal dysfunction typical of idiopathic Parkinson's disease.
16 substitution at codon 2019 (Gly2019 ser), in idiopathic Parkinson's disease.
17 physiology of resting and postural tremor in idiopathic Parkinson's disease.
18 ut the Lewy body pathology characteristic of idiopathic Parkinson's disease.
19 e and a clinical syndrome closely resembling idiopathic Parkinson's disease.
20 diseases, including Alzheimer's disease and idiopathic Parkinson's disease.
21 ly indistinguishable from most patients with idiopathic Parkinson's disease.
22 lower than those reported for patients with idiopathic Parkinson's disease.
23 changes reminiscent of those which occur in idiopathic Parkinson's disease.
24 he specific mutation (A53T) in a 40 cases of idiopathic Parkinson's disease, 3 cases of multisystem a
26 pared to controls persisted in patients with idiopathic Parkinson's disease (after exclusion of all G
27 ganglia was investigated in 25 patients with idiopathic Parkinson's disease and 14 matched healthy co
30 e non-demented subjects with newly diagnosed idiopathic Parkinson's disease and 37 healthy matched co
31 movement have been studied in patients with idiopathic Parkinson's disease and age-matched healthy i
32 sess variant frequencies in individuals with idiopathic Parkinson's disease and controls, matched for
33 idal disorders: idiopathic torsion dystonia, idiopathic Parkinson's disease and Huntington's disease,
34 predictive potential to discriminate between idiopathic Parkinson's disease and Parkinson's disease l
35 solated from control subjects, patients with idiopathic Parkinson's disease and Parkinson's disease p
36 al mitophagy, a process with strong links to idiopathic Parkinson's disease, and demonstrates that ph
37 resynaptic dopamine storage in patients with idiopathic Parkinson's disease as a function of the cate
38 Eligible patients were aged 25-75 years, had idiopathic Parkinson's disease as measured by Queen Squa
39 ing network structure in 37 individuals with idiopathic Parkinson's disease, both ON and OFF dopamine
40 en described with a phenotype much closer to idiopathic Parkinson's disease, but it does not appear t
41 how that fibroblasts from five patients with idiopathic Parkinson's disease can be efficiently reprog
43 tation and clinical features consistent with idiopathic Parkinson's disease, carriers of the autosoma
45 d DJ-1 to be an abundant protein in control, idiopathic Parkinson's disease, cases with clinical and
47 (r -0.66, 95% CI -0.88 to -0.20; p=0.0099), idiopathic Parkinson's disease cohort 1 (r -0.66, -0.84
48 1 (r -0.66, -0.84 to -0.36; p=0.00031), and idiopathic Parkinson's disease cohort 2 (r -0.71, -0.84
49 e also recruited one cohort of patients with idiopathic Parkinson's disease (cohort 1) from Movement
50 gid syndromes of less than 5 years duration: idiopathic Parkinson's disease corticobasal degeneration
51 nts (56 +/- 7 years) suffering from moderate idiopathic Parkinson's disease (disease duration 10 +/-
54 esponses to clonidine clearly differentiated idiopathic Parkinson's disease from MSA-C and MSA-P.
56 ed 86 deceased older Catholic clergy without idiopathic Parkinson's disease from the Religious Order
58 se association between cigarette smoking and idiopathic Parkinson's disease has been reported in seve
60 e, 26 female) cases were diagnosed as having idiopathic Parkinson's disease (IPD) and 70 (42 male, 28
61 lsy (PSP), multiple system atrophy (MSA) and idiopathic Parkinson's disease (IPD) can be clinically i
67 uptake (P = 0.0008) compared with a group of idiopathic Parkinson's disease (IPD) patients who had ba
68 y the role of neuronal complex 1 activity in idiopathic Parkinson's disease (IPD), expression of mito
76 rlier in the cancer trajectory but rarely in Idiopathic Parkinson's Disease(IPD), Progressive Supranu
81 y syndrome, peduncular hallucinosis, treated idiopathic Parkinson's disease, Lewy body dementia witho
82 pars compacta of controls and subjects with idiopathic Parkinson's disease matched for age and postm
83 sed serum GH concentrations in patients with idiopathic Parkinson's disease (median increase 8.98 [IQ
84 tient astrocytes showed CD44 overexpression, idiopathic Parkinson's disease microglia revealed a pro-
86 ingle-nuclei RNA sequencing dataset from the idiopathic Parkinson's disease midbrain, which highlight
88 re to differentiate individual patients with idiopathic Parkinson's disease, multiple system atrophy,
91 nscriptomes of post-mortem midbrain from six idiopathic Parkinson's disease patients and five age-/se
92 duals harbouring mutations in PRKN/PINK1 and idiopathic Parkinson's disease patients remain elusive.
94 nographically, median follow-up: 1.6 years), idiopathic Parkinson's disease (PD) (n=909, median follo
96 peripheral lymphocytes of 43 newly diagnosed idiopathic Parkinson's disease (PD) cases and 62 age- an
97 ny compelling basis for a heritable basis of idiopathic Parkinson's disease (PD) has focused attentio
100 loss of nigral dopaminergic (DA) neurons in idiopathic Parkinson's disease (PD) is believed to resul
102 on of nigrostriatal dopamine (DA) neurons in idiopathic Parkinson's disease (PD) is still unknown.
104 or many years, visual hallucinations (VH) in idiopathic Parkinson's disease (PD) were thought to be a
105 atients with parkinsonian disorders: 86 with idiopathic Parkinson's disease (PD), 30 with progressive
108 sm, and through analysis of a subcohort with idiopathic Parkinson's disease (PD), we have demonstrate
117 thermore, astrocytes and microglia presented idiopathic Parkinson's disease-specific cell proliferati
118 uscles in the forearm of seven patients with idiopathic Parkinson's disease, studied with and without
120 tals, we randomly assigned 299 patients with idiopathic Parkinson's disease to undergo either pallida
121 ver study, 19 patients with mild-to-moderate idiopathic Parkinson's disease underwent functional magn
122 However, Lewy body pathology typical of idiopathic Parkinson's disease was found at autopsy in t
124 esting and postural tremors of patients with idiopathic Parkinson's disease were monitored using tran
126 l as significant reductions in patients with idiopathic Parkinson's disease, which correlates with th
127 eterozygous PRKN/PINK1 mutations compared to idiopathic Parkinson's disease, which is in line with pr
128 -75 years, had been diagnosed with bilateral idiopathic Parkinson's disease with motor symptoms for m
129 age between 22 and 75 years, a diagnosis of idiopathic Parkinson's disease with over 5 years of moto
131 d the effects of clonidine on 14 people with idiopathic Parkinson's disease (without autonomic defici
132 nucleus (STN DBS) improves motor symptoms in idiopathic Parkinson's disease, yet the mechanism of act