ライフサイエンスコーパス: cuprizone

1 xposing these mutants and normal siblings to cuprizone.

2 could be carefully controlled using a toxin, cuprizone.

3 and IGF-1 tg mice 3 weeks after exposure to cuprizone.

4 IP-1alpha knockout mice (MIP-1alpha(-/-)) to cuprizone and comparing pathology to wild-type mice.

5 ain during cuprizone toxicity, mice were fed cuprizone and evaluated at 3-, 4-, and 6-week cuprizone

6 demyelination by feeding the copper chelator cuprizone, and correlated our results with detailed hist

7 phodiesterase-EGFP(+) mice were treated with cuprizone, and OPCs were sorted from the corpus callosum

8 chronically demyelinated lesions induced by cuprizone appears to be the result of oligodendrocyte de

9 ction of BDNF on OLG lineage cells following cuprizone, BDNF(+/-) mice were evaluated.

10 In cuprizone-challenged mice, substantial numbers of NPCs m

11 C57BL/6J mice were maintained on a cuprizone-containing or control diet and sacrificed at s

12 C57BL/6 mice were given 0.2% cuprizone (CPZ) for 2 to 6 weeks while controls ate the

13 Cuprizone (CPZ) is a neurotoxic agent acting as a copper

14 Using the cuprizone (CPZ) model of demyelination and mice of eithe

15 in a non-T-cell model of demyelination, the cuprizone (cupr) model in C57BL/6 mice.

16 ntify myelin loss in brain tissues using the cuprizone demyelination model.

17 as Ind-Cl increased remyelination within the cuprizone diet-induced demyelinating model.

18 cells undergo apoptosis if mice remain on a cuprizone diet.

19 Following cuprizone-elicited demyelination in mice, astrocytes con

20 es, but also oligodendrocytes, in short-term cuprizone-exposed mice.

21 In cuprizone-fed mice, IL-17 was produced by CNS CD3(+) T c

22 nd Th17 CD4(+) T cells infiltrate the CNS of cuprizone-fed mice, with infiltration of Th17 cells bein

23 neration and loss compared to non-irradiated cuprizone-fed mice.

24 For mice of susceptible strains, cuprizone feeding results in oligodendrocyte cell loss a

25 d with that in wild-type mice in response to cuprizone feeding, demonstrating the essential role of I

26 lly demyelinated lesion of mice treated with cuprizone for 12 weeks, mature oligodendrocyte regenerat

27 cuprizone for 27 days and mice that were fed cuprizone for 25 days, followed by normal diet for 2 day

28 brains from control mice, mice that were fed cuprizone for 27 days and mice that were fed cuprizone f

29 dant in the brains of mice that had consumed cuprizone for 27 days, and the numbers of O4-positive ce

30 Female C57BL/6 mice were fed cuprizone for 3 weeks, followed by a period of 2 weeks o

31 ollowing exposure to the demyelinating agent cuprizone, however, GALC +/- animals had significantly r

32 ecific chelators (bathocuproine disulfonate, cuprizone) induced nondesensitizing NMDAR currents even

33 ntiation in fibronectin aggregate containing cuprizone-induced demyelinated lesions in male mice.

34 linated axons and oligodendrocyte numbers in cuprizone-induced demyelinated lesions.

35 trated that n-3 PUFA supplementation reduced cuprizone-induced demyelination and improved motor and c

36 the Nlrp3 gene was increased >100-fold in a cuprizone-induced demyelination and neuroinflammation mo

37 eceptor (CXCR2) were relatively resistant to cuprizone-induced demyelination and that circulating CXC

38 Cuprizone-induced demyelination in mice is a frequently

39 These data suggest that cuprizone-induced demyelination is useful for modeling c

40 ly study its effects on remyelination in the cuprizone-induced demyelination model and in experimenta

41 Cuprizone-induced demyelination remains incompletely cha

42 the present study, we used a murine model of cuprizone-induced demyelination to broaden the applicati

43 l delay, myelination at the onset and during cuprizone-induced demyelination was unaffected in male N

44 ans with multiple sclerosis and of mice with cuprizone-induced demyelination, in ex vivo models of de

45 We show that during cuprizone-induced demyelination, in vivo CXCR7 antagonis

46 Our findings support a two-hit process of cuprizone-induced demyelination, supporting the idea tha

47 he corpus callosi (CCs) of mice subjected to cuprizone-induced demyelination.

48 xamined the importance of IL-17 signaling in cuprizone-induced demyelination.

49 of CNS resident cells in the pathogenesis of cuprizone-induced demyelination.

50 of IL-17-induced Act1-mediated signaling in cuprizone-induced demyelination.

51 us callosum of mice infused with BMP4 during cuprizone-induced demyelination.

52 XCR2-positive neutrophils were important for cuprizone-induced demyelination.

53 s accelerated in lysophosphatidylcholine- or cuprizone-induced demyelination.

54 yelin repair as well as motor recovery after cuprizone-induced demyelination.

55 tion followed by longitudinal studies in the cuprizone-induced demyelination/remyelination mouse mode

56 tive demyelinating MS lesions, as well as in cuprizone-induced lesions, and that this phosphorylation

57 Evidence from a cuprizone-induced model of demyelination, in vitro and i

58 SOCS3-deficient mice were protected against cuprizone-induced oligodendrocyte loss relative to wild-

59 he molecular and cellular mechanism by which cuprizone induces demyelination remains unclear.

60 Cuprizone inhibits mitochondrial function and induces de

61 l compared to non-transplanted, X-irradiated cuprizone-intoxicated mice.

62 the brain to 40 Gy of X-irradiation prior to cuprizone intoxication and this resulted in a significan

63 lammatory protein-1alpha (MIP-1alpha) during cuprizone intoxication, a model where demyelination of t

64 We demonstrate that after cuprizone intoxication, CCR2-dependent infiltration of m

65 hat continuously express IGF-1 (IGF-1 tg) to cuprizone intoxication.

66 ligodendrocytes, might be interrupted during cuprizone intoxication.

67 ental autoimmune encephalomyelitis (EAE) and cuprizone intoxication.

68 Demyelination on exposure to cuprizone is accompanied by predictable microglial activ

69 ment of an innovative animal model combining cuprizone-mediated demyelination with transfer of myelin

70 okines, among them Cxcl10, Ccl2, and Ccl3 in cuprizone-mediated oligodendrocyte apoptosis.

71 ocyte death and remyelination failure in the cuprizone model (male mice).

72 lesion to a chronic state, we have used the cuprizone model of chronic demyelination.

73 The neurotoxicant-induced, cuprizone model of demyelination is ideally suited for t

74 Using the cuprizone model of demyelination, a noninflammatory mode

75 In this study, we used the cuprizone model of demyelination, characterized by oligo

76 (-/-) and Nlrp3(-/-) mice are studied in the cuprizone model of neuroinflammation and demyelination.

77 In the cuprizone model of oligodendrocyte degeneration and demy

78 In this study, we used the cuprizone model to investigate the temporal and causal r

79 in the repair of a demyelinating lesion, the cuprizone model was used and the corpus callosum was exa

80 In the cuprizone model, acute disease reduces serum cholesterol

81 of neuroinflammatory lesions in vivo in the cuprizone mouse model of MS.

82 lin pathology in primary cultures and in the cuprizone mouse model of multiple sclerosis (MS), a deva

83 Using the cuprizone mouse model, we combined electrophysiological

84 The cuprizone neurotoxicant model causes extensive corpus ca

85 ormal diet following 12 weeks of exposure to cuprizone, remyelination and oligodendrocyte regeneratio

86 icient mice, resulting in an amelioration of cuprizone toxicity at later time points.

87 To evaluate Axl's role in brain during cuprizone toxicity, mice were fed cuprizone and evaluate

88 in prolonged axonal damage and recovery from cuprizone toxicity.

89 ion were performed on the corpus callosum of cuprizone treated mice.

90 n vivo on an 11.7T animal MRI scanner from 7 cuprizone-treated and 7 control capital ES, Cyrillic57BL

91 Significant (p < 0.05) demyelination in cuprizone-treated animals was found according to both LF

92 ong-term locomotor performance of previously cuprizone-treated animals was monitored using the motor

93 Moreover, we found that in cuprizone-treated mice the detrimental actions of IFN-ga

94 chemokine transcripts in both untreated and cuprizone-treated MIP-1alpha(-/-) mice.

95 e found that OPC-targeted Notch1 ablation in cuprizone-treated Plp-creER Notch1(lox/lox) transgenic m

96 uprizone and evaluated at 3-, 4-, and 6-week cuprizone treatment and 3- and 5-week post-cuprizone wit

97 on of pharmacological HDAC inhibitors during cuprizone treatment and is consistent with in vitro resu

98 on of pharmacological HDAC inhibitors during cuprizone treatment and is consistent with in vitro resu

99 reased as a function of dose and duration of cuprizone treatment and it was detectable prior to obser

100 numerous chemokines were up-regulated during cuprizone treatment in wild-type, C57BL/6 mice.

101 s, and motor recovery after the cessation of cuprizone treatment were compromised.

102 Following cessation of cuprizone treatment, animals showed an initial recovery

103 BDNF protein levels were reduced after cuprizone treatment, suggesting that the demyelinating l

104 At 4-week cuprizone treatment, the corpora callosa of wildtype (WT

105 At 6-week cuprizone treatment, there was significantly more Oil Re

106 d that Sfmbt2 family miRNAs decreased during cuprizone treatment.

107 and persistent demyelination after prolonged cuprizone treatment.

108 ls, suggesting a source of IL-17 in CNS upon cuprizone treatment.

109 ease in the NG2 response at 4 and 5 weeks of cuprizone treatment.

110 Bis-cyclohexanone oxalyldihydrazone (cuprizone) was administered to young adult mice in order

111 emyelination mediated by the copper chelator cuprizone, we evaluated the expression of CXCL12 and its

112 on microscopy determined that at 3-week post-cuprizone withdrawal the number of dystrophic axons and

113 nificantly more SMI-32+ axons at 3-week post-cuprizone withdrawal, indicative of axonal damage in the

114 In Axl-/- corpora callosa, 5-week post-cuprizone withdrawal, the number of mature oligodendrocy

115 lial activation and astrogliosis, and, after cuprizone withdrawal, this activation reproducibly dimin

116 k cuprizone treatment and 3- and 5-week post-cuprizone withdrawal.