ライフサイエンスコーパス: Lewy body disease

1 res were striking and reminiscent of diffuse Lewy body disease.

2 sight into the role of glucocerebrosidase in Lewy body disease.

3 ivity in a pattern characteristic of diffuse Lewy body disease.

4 has been widely used as a diagnostic aid in Lewy body disease.

5 ent probably reflects brainstem and cerebral Lewy body disease.

6 re subsequently found to have autopsy-proven Lewy body disease.

7 or and cognitive deficits similar to diffuse Lewy body disease.

8 imilar mechanisms could be at play in PD and Lewy body disease.

9 Jointly, these disorders are denominated Lewy body disease.

10 of G2019S-associated Parkinson's disease is Lewy body disease.

11 m 12 controls and 6 patients with Incidental Lewy Body Disease.

12 nd in brains of patients with PD and diffuse Lewy body disease.

13 ontribute to alpha-synuclein accumulation in Lewy body disease.

14 in sporadic Parkinson's disease and diffuse Lewy body disease.

15 stent with the limbic (transitional) form of Lewy body disease.

16 of delusions distinguished PSP from diffuse Lewy body disease.

17 rkinson disease and the neocortex of diffuse Lewy body disease.

18 gs support a role for tau copathology in the Lewy body diseases.

19 ion of alpha-synucleinopathy in PD and other Lewy body diseases.

20 for the formation of Lewy bodies in various Lewy body diseases.

21 ogenic pathway for both genetic and sporadic Lewy body diseases.

22 athogenesis of Parkinson's disease and other Lewy body diseases.

23 er of neurodegenerative disorders, including Lewy body diseases.

24 ional diversion of ERK-signaling pathways in Lewy body diseases.

25 em tissues representing the full spectrum of Lewy body diseases.

26 even with Alzheimer's disease (11%), 11 with Lewy body disease (16%) and four with frontotemporal lob

27 Twenty-four patients with Lewy body disease (7 DLB, 8 PD-impaired, and 9 PD-normal

28 heimer disease, cerebrovascular disease, and Lewy body disease accumulate in the brains of older pers

29 rains of AR-JP and idiopathic PD and diffuse Lewy body disease also exhibit increased level of p38.

30 n other amyloid-associated disorders such as Lewy body disease and atypical forms of AD.

31 post-mortem brain samples from patients with Lewy body disease and controls.

32 are little data on the relationship between Lewy body disease and mild cognitive impairment syndrome

33 On autopsy, six had neocortical-predominant Lewy body disease and two had limbic-predominant Lewy bo

34 rative diseases such as Alzheimer's disease, Lewy body disease, and frontotemporal lobar degeneration

35 body variant of Alzheimer's disease, diffuse Lewy body disease, and Parkinson's disease and suggests

36 body variant of Alzheimer's disease, diffuse Lewy body disease, and Parkinson's disease, NACP was fou

37 throughout the striatum in individuals with Lewy body disease, and serotonergic degeneration in huma

38 dually varying mixture of Alzheimer disease, Lewy body disease, and vascular brain injury.

39 e therapeutic imperative for Alzheimer's and Lewy body diseases, and provide evidence to support the

40 id deposits, the alpha-synuclein deposits in Lewy body diseases are intracellular, and thus it is les

41 ism, sporadic Parkinson disease, and diffuse Lewy Body disease as well as the 1-methyl-4-phenyl-1,2,3

42 Alzheimer disease with or without concurrent Lewy body disease as well as three cellular models of pr

43 d to the development of a staging system for Lewy body disease-associated pathological changes.

44 s disease pathology frequently coexists with Lewy body disease at autopsy in patients with probable d

45 increase in transcription of 4-repeat tau in Lewy body disease brains.

46 ted regions in Parkinson disease and diffuse Lewy body disease brains.

47 ntribute to the pathogenesis of PD and other Lewy body diseases by promoting alterations in parkin an

48 eptides may contribute to the development of Lewy-body diseases by promoting the aggregation of alpha

49 mately 2% (n = 8) of our Parkinson's disease/Lewy body disease cases (n = 405).

50 Alzheimer's/Parkinson's disease and diffuse Lewy body disease cases had significantly higher amounts

51 These findings indicate that among Lewy body disease cases that pass through a mild cogniti

52 ases with pathologically defined neocortical Lewy body disease confirmed the link between bradykineti

53 poral degeneration (FTD) (n = 9), or diffuse Lewy body disease (DLB) with mixed AD or FTD pathologies

54 s Parkinson's disease (PD) and dementia with Lewy body disease (DLB).

55 hallmark of Parkinson's disease and diffuse Lewy body disease (DLBD) is the aggregation of alpha-syn

56 ed from postmortem human brains with diffuse Lewy body disease (DLBD) preferentially show endocytosis

57 ts with an AD-like dementia known as diffuse Lewy-body disease (DLBD).

58 ody variant of AD [LBVAD] and 4 pure diffuse Lewy body disease [DLBD]) who had antemortem position em

59 If this topography and temporal evolution of Lewy body disease does occur, other manifestations of th

60 early stage PD cases and cases of incidental Lewy body disease (ILBD), which is thought to represent

61 s a predictable topography of progression of Lewy body disease in the CNS, beginning in olfactory str

62 ly to neurons in the brains of patients with Lewy body disease, in co-transduced cells alpha-synuclei

63 were eventually shown to have autopsy-proven Lewy body disease, indicating that rapid eye movement sl

64 ve disorders such as Parkinson's disease and Lewy body disease is increased upon injury to the nervou

65 We conclude that sympathetic denervation in Lewy body diseases is associated with decreased vesicula

66 hat occur in Parkinson's disease and related Lewy body diseases is essential for development of new t

67 A poorly understood feature of Lewy body diseases is loss of sympathetic nerves in the

68 NAs are differentially affected in brains of Lewy body disease (LBD) and Alzheimer's disease (AD) pat

69 D) neuropathologic changes (NCs) but without Lewy body disease (LBD) NCs (AD group; n=244), dementia

70 s a hallmark of Parkinson's disease (PD) and Lewy body disease (LBD), a heterogeneous group of disord

71 tes of disease duration in participants with Lewy body disease (LBD).

72 eneration and the characteristic symptoms of Lewy body disease (LBD).

73 c output in pathologically confirmed diffuse Lewy body disease (LBD).

74 egenerated in many patients with early stage Lewy Body Diseases (LBD).

75 A final clinical diagnosis of Lewy-body disease (LBD) or APS was made after a mean fol

76 both classifiers) than those diagnosed with Lewy-body diseases (LBDs; majority Parkinson disease [PD

77 pha-syn has been investigated extensively in Lewy body disease, less is known about the role of this

78 In a transgenic mouse model of diffuse Lewy body disease, long-term administration of phenylbut

79 Conclusions and Relevance: Patients with Lewy body disease manifest a spectrum of tau pathology.

80 entional Lewy pathology suggests that AD and Lewy body disease may be more closely related than previ

81 Here we prioritize as multisystem Lewy body disease (MLBD) those genetic forms of Parkinso

82 ), Parkinson's disease (PD, n = 11), diffuse Lewy body disease (n = 14).

83 body disease and two had limbic-predominant Lewy body disease; only one had coexisting high-likeliho

84 ied with MCI were without "high"-level ADNC, Lewy body disease, or hippocampal sclerosis pathologies;

85 ry, in several conditions including cortical Lewy body disease, Parkinson's disease dementia, traumat

86 e neurodegenerative disorder associated with Lewy body disease pathology in central and peripheral ne

87 ry, but generally the dominant genes cause a Lewy body disease spectrum whereas recessive genes cause

88 was observed in degenerating human Parkinson/Lewy body disease substantia nigra neurons but not in ag

89 id fibrils that underlie the pathogenesis of Lewy body diseases such as Parkinson's disease.

90 Alzheimer's/Parkinson's disease, and diffuse Lewy body disease) using in situ end labeling to detect

91 lele in AD subjects with concomitant diffuse Lewy body disease was intermediate between controls and

92 aline atherosclerosis, siderocalcinosis, and Lewy body disease were independently associated with cog

93 el mechanism for epigenetic dysregulation in Lewy body diseases, which might underlie the decrease in

94 inding was observed in 4 of 17 patients with Lewy body disease with low cortical [11C]PiB retention.

95 patients with pure autonomic failure (PAF, a Lewy body disease without parkinsonism); in patients wit