ライフサイエンスコーパス: chorea

1 tem was Streptococcus pyogenes in Sydenham's chorea.

2 oclonal antibody 24.3.1 and sera from active chorea.

3 correlation with Vonsattel score except for chorea.

4 isorder, and therefore similar to Sydenham's chorea.

5 te the dominant loss of striatal neurons and chorea.

6 e patients had rheumatic fever or Sydenham's chorea.

7 nting with dominant parkinsonism and minimal chorea.

8 inhibitory neurons are involved, also their chorea.

9 None had rheumatic fever or Sydenham's chorea.

10 me, as well as rheumatic fever or Sydenham's chorea.

11 manent basal ganglia dysfunction might cause chorea.

12 on and increasing motor impairments, but not chorea.

13 the BG, is characterized by hyperkinesia and chorea.

14 ollowed by dysarthria, dysphagia, ataxia, or chorea.

15 aviors and involuntary movements in Sydenham chorea.

16 nical features of HD, including dystonia and chorea.

17 provement in dystonia against aggravation of chorea.

18 Most remarkable were the high frequencies of chorea (11%) and cranial neuropathy (17%, including 10%

19 It has been hypothesized that Sydenham's chorea, a major manifestation of rheumatic fever, may pr

20 nes result in a variety of diseases, such as chorea acanthocytosis (ChAc), but the cellular functions

21 tic anemia and resembling the human disorder chorea acanthocytosis.

22 generative hereditary disorders that include chorea-acanthocytosis (ChAc) and McLeod syndrome (MLS).

23 Chorea-acanthocytosis (ChAc) is a fatal neurodegenerativ

24 Chorea-acanthocytosis (ChAc) is a fatal neurological dis

25 Chorea-acanthocytosis (ChAc) is a severe, neurodegenerat

26 The rare human disorder chorea-acanthocytosis (ChAc) is caused by mutations in h

27 The gene mutated in chorea-acanthocytosis (CHAC; approved gene symbol VPS13A

28 axias, dentatorubral-pallidoluysian atrophy, chorea-acanthocytosis and iron-accumulation disorders.

29 ion of active Lyn and autophagy was found in chorea-acanthocytosis based on Lyn coimmunoprecipitation

30 In chorea-acanthocytosis erythrocytes, active Lyn is seques

31 n associated with Atg7 in healthy but not in chorea-acanthocytosis erythrocytes.

32 Our results uncover in chorea-acanthocytosis erythroid cells an association bet

33 Chorea-acanthocytosis is characterized by circulating ac

34 Chorea-acanthocytosis is one of the hereditary neurodege

35 ed K+ channel genes, KCNA5 and KCNA6; 6) the chorea-acanthocytosis locus on 9q21; 7) the Huntington-l

36 In addition, reticulocyte-enriched chorea-acanthocytosis red cell fractions exhibited delay

37 We report here for the first time that chorea-acanthocytosis red cells are characterized by imp

38 es and membrane remnants only in circulating chorea-acanthocytosis red cells.

39 In chorea-acanthocytosis, we found (1) dyserythropoiesis; (

40 sease is uncontrolled involuntary movements (chorea) accompanied by progressive cognitive and psychia

41 que clinical presentation of childhood-onset chorea and characteristic brain MRI showing symmetrical

42 ar after Charcot's death, Osler published On Chorea and Choreiform Affectations (1894), and in this p

43 sing CB1 levels are strongly correlated with chorea and cognitive deficit.

44 n patients with Parkinson's disease (PD) are chorea and dystonia, and often the two types are intermi

45 isorder with a distinct phenotype, including chorea and dystonia, incoordination, cognitive decline,

46 Chorea and dystonia, usually in the legs, occur less com

47 with various diseases, including Huntington chorea and fragile X syndrome.

48 t Charcot had failed to separate, Sydenham's chorea and Huntington's disease.

49 ive neurologic diseases such as Huntington's chorea and late-stage Parkinson disease.

50 ified Neurological Examination (QNE) and its chorea and motor impairment subscales, the Mini-Mental S

51 11 regions containing genes associated with chorea and myokymia: 1) the Huntington disease gene on c

52 Sydenham's chorea and other central nervous system illnesses that a

53 mising etiologically targeted treatments for chorea and other hyperkinetic movement disorders.

54 of autoimmune movement disorders [Sydenham's chorea and PANDAS (pediatric autoimmune neuropsychiatric

55 been described in association with dystonia, chorea and parkinsonism.

56 bodies (ABGA) are associated with Sydenham's chorea and pediatric autoimmune neuropsychiatric disorde

57 es are directed at managing symptoms such as chorea and psychiatric disturbances.

58 mAbs 24.3.1, 31.1.1, and 37.2.1 derived from chorea and selected for cross-reactivity with group A st

59 naling in the immunopathogenesis of Sydenham chorea and will lead to a better understanding of other

60 a hyperkinetic score, combining dystonia and chorea, and (2) a hypokinetic score, combining bradykine

61 n with PANDAS, nine children with Sydenham's chorea, and 24 healthy children were evaluated for D8/17

62 isease,movement disorders, ataxia, dystonia, chorea, and Creutzfeldt-Jakob with and Jewish.

63 and early-onset ataxia with a rapid course, chorea, and dementia.

64 including Alzheimer's disease, Huntington's chorea, and glial tumor; however, the precise function o

65 nted with acute-onset confusion, opsoclonus, chorea, and intractable seizures.

66 riable phenotype including ataxia, dystonia, chorea, and parkinsonism, as well as cognitive impairmen

67 s exhibit neuronal dysfunction/degeneration, chorea, and progressive weight loss.

68 t disorders (parkinsonism, dystonia, tremor, chorea, and restless legs syndrome) were included.

69 ed expression in rheumatic fever, Sydenham's chorea, and subgroups of obsessive-compulsive disorder a

70 rs such as Parkinson's disease, Huntington's chorea, and tardive dyskinesia arise from an imbalance b

71 araneoplastic, such as anti-CRMP5-associated chorea, anti-Ma2 hypokinesis and rigidity, anti-Yo cereb

72 Chorea antibodies targeted the surface of human neuronal

73 inhibited is consistent with the theory that chorea arises from selective degeneration of striatal pr

74 d movement disorder (opsoclonus, ataxia, and chorea) as well as seizures refractory to treatment.

75 enazine to deutetrabenazine in patients with chorea associated with Huntington disease (HD).

76 Among patients with chorea associated with Huntington disease, the use of de

77 of hyperkinetic movement disorders including chorea, ballism, athetosis, dystonia, tremor, myoclonus,

78 ) encephalitis, which may cause dyskinesias, chorea, ballismus or dystonia (NMDAR antibodies), the sp

79 These include migraine, encephalopathy, chorea, brain stem dysfunction, myelopathy, mononeuritis

80 the hallmark autoimmune disorder Sydenham's chorea, but PANDAS remains controversial.

81 cal activity correlated with the severity of chorea, but SMR and total energy expenditure did not.

82 Tourette's syndrome, rather than Sydenham's chorea, but who have similar poststreptococcal autoimmun

83 rted at the age of 3 to 4 years and included chorea, cerebellar ataxia, dystonia, and pyramidal tract

84 ade, and symptom scores of motor impairment, chorea, cognition, and mood.

85 ound previously for subjects with Sydenham's chorea compared with normal subjects.

86 NDAS and 89% of the children with Sydenham's chorea, compared with 17% of the healthy children, were

87 Chorea control, as measured by the total maximal chorea

88 e was titrated on a weekly basis for optimal chorea control.

89 le safety profile and effectively maintained chorea control.

90 Tetrabenazine is efficacious for chorea control; however, tolerability concerns exist.

91 in Huntington disease (HD), characterized by chorea, dementia and severe weight loss, culminating in

92 ary neurodegenerative disorder that produces chorea, dementia, and death.

93 idlife onset of debilitating and progressive chorea, dementia, and psychological disturbance.

94 Reactivity of chorea-derived mAb 24.3.1 or SC IgG with D2R was confirm

95 her streptococcal diseases in the absence of chorea did not activate the kinase.

96 ition, there are recent reports of dystonia, chorea encephalopathy, and dystonic choreoathetosis occu

97 The presence of opsoclonus, ataxia, and chorea expands the clinical phenotype and indicates that

98 tification of PDE10A mutations as a cause of chorea further motivates the study of cAMP signaling in

99 In Sydenham chorea, human mAbs derived from disease target the group

100 ptoms comprising various elements, including chorea, hyperactivity, tics, emotional lability, and obs

101 ars (SD = 13.3, range 13-63), beginning with chorea in 50%, focal lower limb dystonia in 42.5% and pa

102 the only approved drug for the treatment of chorea in HD, tetrabenazine (TBZ).

103 Citing the use of tetrabenazine for chorea in Huntington disease, adrenocorticotropic hormon

104 ease, with clinical manifestations including chorea, incoordination, ataxia, and dementia.

105 acterized by abnormal involuntary movements (chorea), intellectual impairment and selective neuronal

106 Sydenham's chorea is a CNS disorder and sequela of group A streptoc

107 Chorea is a hyperkinetic movement disorder resulting fro

108 Paraneoplastic chorea is described in 16 patients: 11 with limited smal

109 Sydenham chorea is the major neurological manifestation of ARF bu

110 s on 16p11.2-q11.2; 9) the benign hereditary chorea locus on 14q; 10) the SCA type 5 locus on chromos

111 In addition, chorea mAb 24.3.1 and acute chorea sera induced calcium/

112 Chorea mAb specificity for purified brain tubulin was co

113 Nucleotide sequence analysis of the chorea mAb V(H) genes revealed that mAb 24.3.1 V(H) gene

114 The chorea mAbs labeled both intra- and extracellular Ags of

115 Our novel findings reveal that Sydenham's chorea mAbs target a 55-kDa brain protein with an N-term

116 Lysoganglioside G(M1) inhibited binding of chorea mAbs to tubulin and mAb reactivity with human cau

117 bitory effect for patients with little or no chorea may be due to additional degeneration of projecti

118 ter 27 AIds; the highest SIRs were noted for chorea minor (8.00), lupoid hepatitis (5.75), and Addiso

119 Chorea monoclonal antibodies showed specificity for mamm

120 despite the absence of documented Sydenham's chorea or rheumatic fever.

121 Other disorders such as Sydenham's chorea, or chorea related to systemic lupus erythematosu

122 In patients with chorea, overnight conversion to deutetrabenazine therapy

123 Patients had dystonia, chorea, parkinsonism, dysarthria, dysphagia, seizures, c

124 y recurrent and brief attacks of dystonia or chorea precipitated by sudden movements.

125 lies including mental retardation, dystonia, chorea, pyramidal signs and a compulsive and aggressive

126 ther disorders such as Sydenham's chorea, or chorea related to systemic lupus erythematosus and antip

127 nged contractions that may contribute to the chorea, rigidity, and dystonia that characterize Hunting

128 Chorea, rigidity, dystonia, and muscle weakness are char

129 ead to disease in disorders such as Sydenham chorea (SC) is not known.

130 tington's Disease Rating Scale total maximal chorea score and total motor score were efficacy end poi

131 Primary end point was the total maximal chorea score change from baseline (the average of values

132 tington disease and a baseline total maximal chorea score of 8 or higher (range, 0-28; lower score in

133 ea control, as measured by the total maximal chorea score, was maintained at week 1 and significantly

134 utetrabenazine group, the mean total maximal chorea scores improved from 12.1 (95% CI, 11.2-12.9) to

135 h their sensitivity in diagnosing Sydenham's chorea seems excellent, it is not yet possible to extrap

136 vels of anti-tubulin IgG were found in acute chorea sera and cerebrospinal fluid.

137 In addition, chorea mAb 24.3.1 and acute chorea sera induced calcium/calmodulin-dependent protein

138 rt disease and the neuronal cell in Sydenham chorea share a common streptococcal epitope GlcNAc and t

139 movements, including motor restlessness and chorea, slowing of voluntary movements and cognitive imp

140 hogenic role of autoantibodies in Sydenham's chorea, the prototypic post-streptococcal neuropsychiatr

141 Other than chorea, tics and obsessive-compulsive disorder, which co

142 ovement disorders include tremors, dystonia, chorea, tics, myoclonus, stereotypies, restless legs syn

143 Osler's On Chorea uniquely captures the transition period between t

144 Two had early Parkinsonian tremor and chorea was seen in four, although in two this was attrib

145 Chorea was the initial and most prominent symptom in 11

146 tetrabenazine, a novel molecule that reduces chorea, was well tolerated in a double-blind, placebo-co

147 t Huntington's disease patients with greater chorea were disinhibited is consistent with the theory t

148 Human mAbs and autoantibodies in Sydenham chorea were found to signal neuronal cells and activate

149 her (range, 0-28; lower score indicates less chorea) were enrolled from August 2013 to August 2014 an

150 The mice develop progressive chorea with onset at approximately 9 weeks of age and wi

151 by 3.0 points (95% CI, 2.5-3.4) per year and chorea worsened by 0.3 point per year (95% CI, 0.1-0.5).