ライフサイエンスコーパス: cerebellar degeneration

1 cognitive and motor dysfunctions arise from cerebellar degeneration.

2 ectrin causes progressive motor deficits and cerebellar degeneration.

3 l dominant spinocerebellar ataxias (SCAs) is cerebellar degeneration.

4 essive cerebellar ataxia and marked isolated cerebellar degeneration.

5 the anti-Tr immune response in patients with cerebellar degeneration.

6 n improve motor performance of patients with cerebellar degeneration.

7 neuronal excitability in the pathogenesis of cerebellar degeneration.

8 fferent cell types to fully recapitulate the cerebellar degeneration.

9 ere described 10 years ago in paraneoplastic cerebellar degeneration.

10 ce develop a strong ataxia in the absence of cerebellar degeneration.

11 mice exhibit neither Dpl overexpression nor cerebellar degeneration.

12 ssociated with tumor immunity and autoimmune cerebellar degeneration.

13 y postural abnormalities, motor deficits and cerebellar degeneration.

14 entified as an autoantigen in a patient with cerebellar degeneration.

15 ovarian and breast, can cause paraneoplastic cerebellar degeneration.

16 clerosis, hereditary spastic paraplegia, and cerebellar degenerations.

17 Twenty-five patients with paraneoplastic cerebellar degeneration (44%) had high titres of HuAb, f

18 in ataxia-telangiectasia, is associated with cerebellar degeneration, abnormal proliferation of small

19 ural-specific deletion of FIP200 resulted in cerebellar degeneration accompanied by progressive neuro

20 of death of 65% HuAb positive paraneoplastic cerebellar degeneration and 10% HuAb negative paraneopla

21 essive disorder characterized by progressive cerebellar degeneration and a greatly increased incidenc

22 A man in his 30s with paraneoplastic cerebellar degeneration and anti-Tr underwent treatment

23 esent a patient who developed paraneoplastic cerebellar degeneration and anti-Yo antibody response in

24 sidered in patients presenting with subacute cerebellar degeneration and anti-Yo antibody response in

25 eveloped neurological disease, and exhibited cerebellar degeneration and BG process loss.

26 with progressive loss of miRNAs, followed by cerebellar degeneration and development of ataxia.

27 ed normally but acquired severe ataxia, with cerebellar degeneration and gliosis.

28 e response is associated with paraneoplastic cerebellar degeneration and Hodgkin lymphoma (HL).

29 in a number of clinical symptoms, including cerebellar degeneration and increased cancer predisposit

30 , comparing the performance of patients with cerebellar degeneration and matched controls.

31 Nineteen human subjects with pure cerebellar degeneration and matched healthy controls wer

32 we studied the cerebellum of 9 patients with cerebellar degeneration and of 9 age-matched normal cont

33 Affected brain tissue showed substantial cerebellar degeneration and tau deposition.

34 oplastic encephalomyelitis, 1 paraneoplastic cerebellar degeneration, and 1 opsoclonus-myoclonus synd

35 elangiectasia-like disorder (ATLD) featuring cerebellar degeneration, and cancer-predisposition in ce

36 inemia of infancy, cardiac long QT syndrome, cerebellar degeneration, and certain ataxias.

37 bations of speech to show that patients with cerebellar degeneration are impaired in adapting feedfor

38 that the hemiplegic migraine attacks and the cerebellar degeneration are linked genetically and that

39 ikingly similar ocular motility findings and cerebellar degeneration are reported in both FHM and a g

40 spinal fluid of patients with paraneoplastic cerebellar degeneration associated with cancer of the ov

41 ibit three distinct defects: (1) progressive cerebellar degeneration associated with severe ataxia, (

42 rataxin (APTX) deficiency causes progressive cerebellar degeneration, ataxia and oculomotor apraxia i

43 .1 restricted epitopes of the paraneoplastic cerebellar degeneration breast/ovarian cancer antigen cd

44 n did not alter the course of paraneoplastic cerebellar degeneration, but improved Lambert-Eaton myas

45 Mutations in TG6 induce cerebellar degeneration by an unknown mechanism.

46 h the same tumour can develop paraneoplastic cerebellar degeneration by different immunological mecha

47 nts afflicted with varying degrees of global cerebellar degeneration caused by hereditary, idiopathic

48 ffered from the HuAb negative paraneoplastic cerebellar degeneration cohort, HuAb positive patients w

49 t the C3H/HeSnJ inbred strain has late onset cerebellar degeneration due to this mutation.

50 ne expression and delayed ATXN1[82]-mediated cerebellar degeneration during mid-stage disease progres

51 Second, individuals with cerebellar degeneration failed to modulate their behavio

52 s with presenting symptoms of paraneoplastic cerebellar degeneration for the presence of HuAb and P/Q

53 nine patients (16%) from both paraneoplastic cerebellar degeneration groups developed electrophysiolo

54 es from 5 other patients with paraneoplastic cerebellar degeneration, HL, and anti-Tr.

55 iectasia (A-T) is a genetic disorder causing cerebellar degeneration, immune deficiency, cancer predi

56 cessive disease characterized by progressive cerebellar degeneration, immunodeficiencies, genomic ins

57 asia (AT) is a recessive syndrome, including cerebellar degeneration, immunologic defects and cancer

58 enerative disease primarily characterized by cerebellar degeneration in children leading to motor imp

59 We tested cerebellar degeneration in human patients in a task desi

60 s of ATM protein is not sufficient to induce cerebellar degeneration in mice.

61 protein (PrPC) rescues doppel (Dpl)-induced cerebellar degeneration in mice.

62 r late onset SCA13, which typically produces cerebellar degeneration in middle age.

63 mal membrane permeabilization contributes to cerebellar degeneration in NPC disease.

64 Even though we found no gross cerebellar degeneration in older Atm(y/y) animals, ectop

65 ne whether gluten sensitivity contributes to cerebellar degeneration in patients with hereditary cere

66 This indicates that cerebellar degeneration is not primarily triggered by lo

67 APT is a subtype of SPT in which progressive cerebellar degeneration is the most symptomatic feature.

68 isorder in which patients show a progressive cerebellar degeneration leading to ataxia, abnormal eye

69 with small-cell lung cancer, paraneoplastic cerebellar degeneration may occur with or without Hu ant

70 (ALC), 8 with (ACD) and 9 without alcoholic cerebellar degeneration (non-ACD).

71 ion does not mirror the localized pattern of cerebellar degeneration observed in tg(la) mice, providi

72 Because patients with cerebellar degeneration often show substantial atrophy o

73 These results suggest there is an effect of cerebellar degeneration on primary auditory function.

74 ecifically, we examined the effect of global cerebellar degeneration on primary auditory sensory func

75 cal developments, focusing on paraneoplastic cerebellar degeneration, opsoclonus-myoclonus, and encep

76 In other disorders, such as paraneoplastic cerebellar degeneration or paraneoplastic sensory neuron

77 g the motor command in perturbed trials, and cerebellar degeneration participants were not.

78 ual information about hand position affected cerebellar degeneration patients (N = 12) and age-matche

79 eration and 10% HuAb negative paraneoplastic cerebellar degeneration patients (P < 0.001).

80 ddition, 20% of HuAb negative paraneoplastic cerebellar degeneration patients without clinically iden

81 tive and 20% of HuAb negative paraneoplastic cerebellar degeneration patients, the tumour was either

82 eral blood of two HLA-A2.1(+) paraneoplastic cerebellar degeneration patients.

83 For example, patients with paraneoplastic cerebellar degeneration (PCD) appear to suppress the gro

84 r described autoantibodies in paraneoplastic cerebellar degeneration (PCD) combined with Hodgkin lymp

85 Except for paraneoplastic cerebellar degeneration (PCD) in HL and dermato/ polymyo

86 Paraneoplastic cerebellar degeneration (PCD) is a disorder in which bre

87 Paraneoplastic cerebellar degeneration (PCD) is believed to be an autoi

88 Patients with paraneoplastic cerebellar degeneration (PCD) offer the opportunity to e

89 Patients with paraneoplastic cerebellar degeneration (PCD) provide an opportunity to

90 sera was used previously to identify several cerebellar degeneration-related (cdr) genes encoding put

91 icted to thymic stromal cells that expressed cerebellar degeneration-related Ag 1 and lacked expressi

92 esults also show that to develop progressive cerebellar degeneration requires expressing ATXN1 with a

93 ts with Hodgkin's disease and paraneoplastic cerebellar degeneration resulted in the isolation of MAZ

94 characterized by ataxia, severe progressive cerebellar degeneration, seizures, uncontrollable moveme

95 ich's ataxia as well as those with intrinsic cerebellar degeneration showed the above abnormalities,

96 Furthermore, paraneoplastic cerebellar degeneration sometimes occurs in association

97 (Parkinson's disease, n = 9), patients with cerebellar degeneration [spinocerebellar ataxia (SCA) ty

98 ed with different cancers and paraneoplastic cerebellar degeneration suggests that several immunologi

99 us animals, which show no signs of ataxia or cerebellar degeneration up to 2 years of age.

100 A-T is characterized by progressive cerebellar degeneration, variable immunodeficiency, and

101 of these disorders present with progressive cerebellar degeneration, whereas the third presents with

102 Patients with paraneoplastic cerebellar degeneration who were HuAb positive were comp