ライフサイエンスコーパス: Pick's disease

1 to control and other FTLD-tau (for example, Pick's disease).

2 ith pathological tau protein accumulation in Pick's disease.

3 inding repeat, detected other tau lesions in Pick's disease.

4 tations were identified in separate cases of Pick's disease.

5 gene in 30 cases of pathologically confirmed Pick's disease.

6 neuropathological studies on a patient with Pick's disease.

7 chromosome 17 (FTDP-17), historically termed Pick's disease.

8 instability successfully classified PSP from Pick's disease.

9 eration, progressive supranuclear palsy, and Pick's disease.

10 nuclear palsy, corticobasal degeneration and Pick's disease.

11 nce our understanding of the pathobiology of Pick's disease.

12 generation and acetylation on Lysine 311 for Pick's disease.

13 e expression of other markers was highest in Pick's disease.

14 t different conformations in Alzheimer's and Pick's diseases.

15 sy with clinical frontotemporal dementia, 33 Pick's disease, 12 FTLD-MAPT and 52 control brains to ch

16 rom 338 people with pathologically confirmed Pick's disease (205 [61%] male and 133 [39%] female; 338

17 tau filaments from Alzheimer's disease(1,2), Pick's disease(3), chronic traumatic encephalopathy(4) a

18 ly had a lower pTau protein load compared to Pick's disease across tau epitopes.

19 generation/progressive supranuclear palsy or Pick's disease and 89% of semantics had TDP(C).

20 ntia (FTD), S320F mutant tau associated with Pick's disease and a combinatorial approach using P301L/

21 ), temporofrontal but not parietal cortex in Pick's disease and all three lobes with ADNC or TDP(A).

22 y heterogeneous; while pathologically proven Pick's disease and corticobasal degeneration were clinic

23 tients with other lobar dementias, including Pick's disease and corticobasal degeneration, by the abs

24 inct from those seen in Alzheimer's disease, Pick's disease and CTE(17-19).

25 mutation and 3-repeat isoforms in brains of Pick's disease and familial tauopathy due to G272V tau m

26 nts in 149 patients and 50 controls from the PIck's disease and Progressive supranuclear palsy Preval

27 anuclear palsy, corticobasal degeneration or Pick's disease), and 69 with FTLD and TDP inclusions (FT

28 luding progressive supranuclear palsy (PSP), Pick's disease, and Alzheimer's disease.

29 s, including progressive supranuclear palsy, Pick's disease, and Alzheimer's disease.

30 f Tau fibers in three distinct diseases, AD, Pick's disease, and chronic traumatic encephalopathy, re

31 ive diseases-progressive supranuclear palsy, Pick's disease, and corticobasal degeneration-illustrate

32 eimer's disease, cortico-basal degeneration, Pick's disease, and frontotemporal lobe degeneration.

33 t are distinct from those of Alzheimer's and Pick's diseases, and from those formed in vitro(12-15).

34 Pick body-positive Pick's disease appeared three times.

35 The filaments of Pick's disease are loosely arranged in pathognomonic sph

36 eration, progressive supranuclear palsy, and Pick's disease, as well as by hereditary frontotemporal

37 The original diagnosis had been of Pick's disease based on frontotemporal atrophy, but re-e

38 l-insoluble gray and white matter regions of Pick's disease brains.

39 to analyze the tau isoform composition in 14 Pick's disease brains.

40 'tauopathies', which include Alzheimer's and Pick's diseases, but tau pathology is also found in the

41 e brain, five chemokines were upregulated in Pick's disease cases (P < 0.0400), consistent with the r

42 lotype was associated with increased risk of Pick's disease compared with the H1 haplotype (OR 1.35 [

43 stinct variety of hyperphosphorylated tau in Pick's disease compromises the long-term viability of se

44 er diagnoses in individual patients included Pick's disease, corticobasal degeneration and other tauo

45 s/nm length, but less dense than AD-PHFs and Pick's disease filaments.

46 e observed at p less than 0.05: with risk of Pick's disease for the H1f subhaplotype (OR 0.11 [0.01 t

47 om individuals with pathologically confirmed Pick's disease from 35 sites (brainbanks and hospitals)

48 (R1, R3, and R4), are found in patients with Pick's disease (frontotemporal dementia).

49 type is associated with an increased risk of Pick's disease in people of European ancestry.

50 osed as having Creutzfeldt-Jakob disease and Pick's disease in the absence of significant neocortical

51 isease (AD) differ from the tau filaments of Pick's disease in their morphology, distribution, and pa

52 utopsy demonstrated the classic pathology of Pick's disease, including massive neuron loss and gliosi

53 The Pick's disease International Consortium provides an oppo

54 tic association study, we used data from the Pick's disease International Consortium, which we establ

55 Pick's disease is a rare and predominantly sporadic form

56 Therefore, Pick's disease is characterized by an accumulations of P

57 Pick's disease is characterized neuropathologically by d

58 Moreover, these data suggest that Pick's disease is not a separate entity but part of the

59 Pick's disease is pathologically defined by the presence

60 Pick's disease (n = 8) and multiple system atrophy (MSA,

61 ve supranuclear palsy neuropathology in 24%, Pick's disease neuropathology in 10%, transactive respon

62 ty of the autopsies in PPA have shown either Pick's disease or lobar atrophy without distinctive hist

63 (P = 0.0345) with the highest expression in Pick's disease (P = 0.0019), while ALDH1L1 was unchanged

64 nction were reduced in FTLD-tau (P = 0.0075; Pick's disease: P < 0.0400) implying astrocyte reactivit

65 tive diseases, particularly tauopathies like Pick's disease (PiD) and Alzheimer's disease (AD), offer

66 in Alzheimer's disease, three-repeat tau in Pick's disease (PiD) and four-repeat tau in progressive

67 of AD, corticobasal degeneration (CBD), and Pick's disease (PiD) brains by Western blots.

68 Pick's disease (PiD) is a rare neurodegenerative disorde

69 tau filaments from Alzheimer's disease (AD), Pick's disease (PiD), and Corticobasal disease (CBD) bra

70 diseases including Alzheimer's disease (AD), Pick's disease (PiD), corticobasal degeneration (CBD), a

71 disease, frontotemporal lobar degeneration, Pick's disease, progressive supranuclear palsy and corti

72 lesions in three other tauopathies including Pick's disease, progressive supranuclear palsy and corti

73 in tauopathies such as Alzheimer's disease, Pick's disease, progressive supranuclear palsy and corti

74 number of other dementing disorders, such as Pick's disease, progressive supranuclear palsy, corticob

75 These include Pick's disease, progressive supranuclear palsy, corticob

76 ological examinations of brains derived from Pick's disease, PSP, and corticobasal degeneration patie

77 ); strongly asymmetric, distributed atrophy (Pick's disease); relatively symmetric, predominantly ext

78 ns of MAPT variants and MAPT haplotypes with Pick's disease risk, age at onset, and disease duration

79 to evaluate the association of MAPT H2 with Pick's disease risk, age at onset, and disease duration.

80 his distinguishes such '4R' tauopathies from Pick's disease (the filaments of which are made of three

81 , nine progressive supranuclear palsy, eight Pick's disease, three frontotemporal dementia with parki

82 PSP, and CBD tissues (K(D)'s = 1-1.5 nM) and Pick's disease tissue (K(D) = 3.8 nM).

83 om Family F had ballooned neurons typical of Pick's disease type B not found in Family D.

84 tau gene mutations are also associated with Pick's disease, we analyzed the tau gene in 30 cases of

85 tter define the spectrum of tau pathology in Pick's disease, we used biochemical, immunohistochemical

86 ilaments differ from those of Alzheimer's or Pick's disease, which have larger cores with different r

87 racterize and compare the filaments found in Pick's disease with those found in AD.

88 This is in contrast to Pick's disease without any tau gene mutations, which con

89 om individuals with pathologically confirmed Pick's disease worldwide.