ライフサイエンスコーパス: MND

1 MND induced apoptosis, inhibited migration and invasion,

2 MND patients commonly displayed an abnormal pattern duri

3 MND SMART is an investigator-led, phase 3, double-blind,

4 MNDs mediate calcium transients in cells with disparate

5 genual anterior cingulate cortex (ACC) in 13 MND and eight control subjects.

6 e neurons provides robust protection against MND, whereas its expression in GFAP-positive glial cells

7 diversification, interventions to alleviate MNDs, such as food fortification(8,9) and biofortificati

8 of German motor neuron disease centers (ALS/MND-NET).

9 iated with better cognitive abilities in ALS/MND, and that a slow brain ageing speed is associated wi

10 uospatial scores (exp(b)=0.625, p<0.009) and MND-FTD (OR=13.75, 95% CI 1.71 to 110.86).

11 es, MNDbi (OR=3.14, 95% CI 1.09 to 8.99) and MND-FTD (OR=5.08, 95% CI 1.26 to 20.40).

12 clinical similarity between this disease and MND seen in other countries.

13 nd the relationship between this disease and MND seen in the rest of the world are still uncertain.

14 ORF72 expansions: 35 had FTD, 16 had FTD and MND, 30 had MND, and three had no clinical phenotype.

15 (47 patients [15 with FTD, nine with FTD and MND, and 23 with MND] and three carriers who had no clin

16 m (40 patients [20 with FTD, 12 with FTD and MND, and eight with MND]), and blood (47 patients [15 wi

17 om 41 patients [21 with FTD, 11 with FTD and MND, and nine with MND]), cerebellum (40 patients [20 wi

18 re the most common genetic cause of FTLD and MND identified to date.

19 verbal fluency and visuospatial scores, and MND-FTD (OR=7.57, 95% CI 1.55 to 46.87).

20 ssion from a pair of vectors, L-tNGFR-SN and MND-tNGFR-SN, indicated that only 1.04% of the CCE cells

21 ens are associated with undernourishment and MNDs.

22 d a significant positive correlation between MND and anti-ketols.

23 ons were not significantly different between MND and control cases, although there were trends toward

24 c FTLD subgroup, and 286 controls or between MND cases and controls.

25 These findings support an overlap between MND, frontotemporal dementia and neuropsychiatric disord

26 rgistic or antagonistic interactions between MNDs, pathogens, and morbidity or mortality relevant to

27 Audit, Research and Evaluation of MND (CARE-MND) register, diagnosed from January 2015 to January 20

28 tion in RNA processing and regulation, cause MNDs and place the dysregulation of RNA pathways at the

29 ked by the discovery of the genes that cause MNDs.

30 that were modified with the human ADA cDNA (MND-ADA) gamma-retroviral vector after conditioning with

31 The Euan MacDonald Centre, MND Scotland, My Name'5 Doddie Foundation, and Baillie G

32 series suggest that pathologically classical MND on Guam may occur independently of neurofibrillary d

33 ited but mostly sporadic, is the most common MND.

34 Micronutrient deficiencies (MNDs) remain widespread among people in sub-Saharan Afri

35 ition, including micronutrient deficiencies (MNDs).

36 or more chronic micronutrient deficiencies (MNDs).

37 ol for studies of motor neuron degeneration (MND).

38 otor neuron disease-frontotemporal dementia (MND-FTD).

39 lthough for most cancer patients who develop MND the occurrence of both disorders is probably coincid

40 Group 3: Six patients developed MND resembling amyotrophic lateral sclerosis between 47

41 sease, is a late-onset motor neuron disease (MND) caused by an abnormal expansion of the CAG repeat i

42 Motor neuron disease (MND) is a common neurodegenerative condition for which t

43 ompounds contribute to motor neuron disease (MND) is supported by association of paraoxonase 1 polymo

44 reports indicate that motor neuron disease (MND) may rarely be associated with systemic cancer.

45 progressive and fatal motor neuron disease (MND) similar to amyotrophic lateral sclerosis (ALS).

46 ssion in patients with motor neuron disease (MND), as tools for future clinical trials, and to probe

47 ondrial dysfunction in motor neuron disease (MND), but the molecular basis of these abnormalities is

48 and 259 patients with motor neuron disease (MND), for whom genomic DNA was available, were investiga

49 Inherited forms of motor neuron disease (MND), including hereditary spastic paraplegias (HSP), ar

50 stological features of motor neuron disease (MND), the term FTLD-MND is used.

51 y occur in people with motor neuron disease (MND), with some studies suggesting an association with t

52 We revealed that motor-neuron disease (MND)-linked RNA-binding proteins (RBPs), TDP-43, FUS, an

53 TLD-U) with or without motor neuron disease (MND).

54 he most common form of motor neuron disease (MND).

55 son's disease (PD) and motor neuron disease (MND).

56 ral dementia (FTD) and motor neuron disease (MND).

57 avioural impairment in motor neuron disease (MND).

58 somal dominant form of motor neuron disease (MND).

59 nctionally abnormal in motor neuron disease (MND, amyotrophic lateral sclerosis), but the nature of t

60 In 2003 the Motor Neurone Disease (MND) Association, together with The Wellcome Trust, fund

61 the high incidence of motor neurone disease (MND) on Guam, and the relationship between this disease

62 tly, 32 patients with motor neurone disease (MND) were studied to identify factors associated with an

63 iologically confirmed motor neurone disease (MND), in whom communication problems were an early and d

64 In motor neurone disease (MND), respiratory muscle weakness causes substantial mor

65 osis (ALS, also called motor neuron disease, MND) are severe neurodegenerative diseases that show con

66 tem for understanding motor neuron diseases (MNDs) and advancing drug discovery.

67 Motor neuron diseases (MNDs) are neurodegenerative disorders that lead to paral

68 Motor neuron diseases (MNDs) are progressive neurodegenerative disorders charac

69 and cellular bases of motor neuron diseases (MNDs) are still poorly understood.

70 Motor neuron diseases (MNDs) encompass an extensive and heterogeneous group of

71 s and dysfunctions in motor neuron diseases (MNDs) such as amyotrophic lateral sclerosis (ALS).

72 sis (ALS) and related motor neuron diseases (MNDs).

73 practice for minor neurocognitive disorder (MND) as well as HAD, despite uncertainty about their acc

74 Motor neuron disorders (MND) include a group of pathologies that affect upper an

75 in mice, which developed normally, displayed MND-like phenotypes after 10 months of age, including ex

76 The story of the 'United to End MND' pound 50m government research funding campaign by t

77 peroxide dismutase 1 (SOD1) related familial MND (fMND).

78 creation of a national DNA Bank specific for MND.

79 d 54.7%, and sensitivity and specificity for MND were 64.3% and 66.0%.

80 d 77.9%, and sensitivity and specificity for MND were estimated at 42.0% and 91.2%.

81 d that long terminal repeat transcripts from MND-CAT-SN are >80 times more abundant than the L-CAT-SN

82 mporal dementia (FTD) with a sister with FTD+MND and the other in a case of progressive non-fluent ap

83 ize-72) in a cohort of individuals with FTD, MND, both these diseases, or no clinical phenotype.

84 D overlapping with motor neuron disease [FTD-MND]), followed by a meta-analysis of the entire dataset

85 wed typical histological appearances of FTLD-MND in two cases and of FTLD-U in one case.

86 FTLD-U or FTLD-MND should be considered in the differential diagnosis o

87 of motor neuron disease (MND), the term FTLD-MND is used.

88 h no family history, who showed a mixed FTLD/MND picture and A324T change in exon 9 was found in two

89 We present a series of 45 cases of Guamanian MND, which reaffirm the clinical similarity between this

90 ions: 35 had FTD, 16 had FTD and MND, 30 had MND, and three had no clinical phenotype.

91 However, MND failed to directly inhibit EGFR or other related rec

92 l layers V (P = 0.003) and VI (P = 0.001) in MND cases compared with controls.

93 neuroimaging and cognitive abnormalities in MND.

94 layer V in the PMC, the DLPFC and the ACC in MND subjects compared with controls [t (19) = 2.91, P =

95 dwide and significantly increase activity in MND genetic research.

96 ss in the PMC and in other cortical areas in MND.

97 tation resulted in a significant decrease in MND and HMND and the simultaneous appearance of ketol di

98 about the timing of cognitive impairment in MND, and whether it arises during early clinically manif

99 tive axonal transport has been implicated in MND and other forms of poly-Q disease.

100 red wines revealed significant increases in MND and anti-ketol contents through aging and a signific

101 etic cascades as being centrally involved in MND, particularly hereditary spastic paraplegia.

102 ducted of the clinical application of NIV in MND among consultant neurologists in the UK.

103 ' as a likely common pathomolecular theme in MND.

104 ment of denervation over short timescales in MND and enables investigation of patterns of disease spr

105 ssed mutated RBP aggregation and toxicity in MND Drosophila models.

106 pid metabolism are known to be implicated in MNDs, there remains a lack of clarity regarding the key

107 IVmnd-2-infected MNDs than SIVmnd-1-infected MNDs.

108 able between SIVmnd-1- and SIVmnd-2-infected MNDs and to those observed in uninfected animals, with t

109 cell counts in chronically SIVmnd-2-infected MNDs than SIVmnd-1-infected MNDs.

110 -producing CD8+ T cells in SIVmnd-2-infected MNDs.

111 n CD4+ T cell counts and VLs in SIV-infected MNDs could be established.

112 erved in another natural host, the mandrill (MND), we conducted a cross-sectional survey of the 23 SI

113 We have previously reported the modified MND LTR (myeloproliferative sarcoma virus enhancer, nega

114 ES and EC cells transduced with the modified MND-CAT-SN vector than in those transduced with L-CAT-SN

115 h frequencies 5-125 Hz, magnetite nanodiscs (MNDs) activate ubiquitous mechano-sensitive calcium sign

116 The formation of 3-methyl-2,4-nonanedione (MND) during red wine aging can contribute to the prematu

117 athy, 41% (9/22) of neuropathy, 22% (2/9) of MND and 63% (5/8) of complex phenotypes were given genet

118 of mitochondrial dysfunction in the cause of MND.

119 tion has confirmed the clinical diagnosis of MND-dementia.

120 EGFR revealed that the biological effects of MND could be abrogated by pertussis toxin.

121 Clinical, Audit, Research and Evaluation of MND (CARE-MND) register, diagnosed from January 2015 to

122 atients with or without clinical evidence of MND.

123 les, providing insight into the evolution of MND, HMND, and ketols through alcoholic fermentation and

124 Pathologically, the classical features of MND were seen in Guamanian Chamorro cases including ubiq

125 teral sclerosis (PLS), a more benign form of MND that only affects upper motor neurons, results in li

126 gnosis, with many occurring independently of MND-FTD and C9orf72 status.

127 However, the occurrence of MND among the indigenous Chamorros of Guam is distinguis

128 ateral sclerosis (ALS) and the occurrence of MND in OP compound-induced delayed neuropathy (OPIDN), i

129 The onset of MND was delayed in these mice compared to the original G

130 In group 2, the proximate onset of MND with the diagnosis of cancer or its recurrence, its

131 ransport during the onset and progression of MND in a line of mice that contained approximately 30% f

132 The classical signs of MND, including wasting, fasciculations and severe bulbar

133 patient with clinical features suggestive of MND but additional cardiac and metabolic symptoms.

134 tion and the clinicopathological syndrome of MND may occur in parallel, observations from this series

135 iation with the dementia/aphasia syndrome of MND suggests that the neural substrate underlying verb r

136 sative gene of a clinically diverse group of MNDs including amyotrophic lateral sclerosis (ALS), atyp

137 disciplinary research on the interactions of MNDs, infection, and inflammation.

138 understanding of the underlying mechanism of MNDs and aid in the development of effective treatments.

139 With the development of mouse models of MNDs, a noninvasive neuroimaging modality capable of det

140 Surveillance of MNDs on the basis of biomarkers of status and dietary in

141 lculated for each scale as a test for HAD or MND.

142 was similar to that from the MND-tNGFR-SN or MND-EGFP-SN vector in nearly all cells, suggesting that

143 ral Sclerosis' OR 'Motor Neuron Disease' OR 'MND'.

144 earch terms were [(motor neuron disease) OR (MND) OR (Amyotrophic Lateral Sclerosis) OR (ALS)] AND [(

145 We also identify how other MND-associated molecules may impact these cascades, in p

146 in hereditary spastic paraplegias and other MNDs.

147 ng functional motor neurons in ALS and other MNDs.

148 NTE pathway disturbances contribute to other MNDs including ALS, and supports the role of NTE abnorma

149 in ALS patients than in patients with other MNDs.

150 -yl)methanone O-2-(diethylamino)ethyl oxime (MND) exhibited the best safety profile.

151 with cognitive and behavioural changes post-MND diagnosis, with many occurring independently of MND-

152 ereby improving their utility in preclinical MND research and therapeutic development.

153 ase SCYL1, causes an early onset progressive MND with characteristic features of amyotrophic lateral

154 ree patients developed a rapidly progressive MND, less prominent symptoms of involvement of other are

155 ctors using either a viral-derived promoter, MND, or the human proximal WAS promoter (WS1.6) for huma

156 and vectors based on our previously reported MND backbone, which has alterations to address three vir

157 These findings support the notion that MND should be considered a multisystem disorder.

158 Mechanistic studies revealed that MND strongly abrogated EGF-induced proliferation, migrat

159 The MND SMART trial aims to test the safety and efficacy of

160 The MND-ADA vector was persistently detected in PBMCs (vecto

161 In group 1, the MND associated with the anti-Hu antibody is unequivocall

162 ed a higher frequency of expression from the MND LTR (20% to 80%) in hematopoietic cells of all linea

163 Expression from the MND LTR reached 88% in thymic T lymphocytes and 54% in s

164 sed slightly to 3% while expression from the MND-EGFP-SN vector persisted in 80% of the cells.

165 rter expression was similar to that from the MND-tNGFR-SN or MND-EGFP-SN vector in nearly all cells,

166 suggest further clinical development of the MND-huWASp LV for a future clinical trial for WAS.

167 tor in nearly all cells, suggesting that the MND vectors are far less susceptible to position-depende

168 Therefore, the MND vector offers an improved vehicle for reliable gene

169 ssion in only 5% of the population while the MND-EGFP-SN vector drove expression in 88% of the cells.

170 pressed the cell surface reporter, while the MND-tNGFR-SN vector drove expression in 99.54% of the CC

171 CD34+ cells were transduced ex vivo with the MND (myeloproliferative sarcoma virus, negative control

172 non-Chamorros who resided on Guam when their MND symptoms occurred.

173 mechanism whereby mutations in SOD1 lead to MND remains enigmatic, we asked whether NF inclusions in

174 s demonstrated that ketols are precursors to MND during red wine oxidation.

175 Together, MND represents a new nonquinazoline potential drug candi

176 Today the primary focus of the UK MND DNA Bank still remains to identify causative and dis

177 , the impacts of genetic variants underlying MND act in a non-cell autonomous manner, instead affecti

178 vey of the 23 SIV-infected and 25 uninfected MNDs from the only semifree colony of mandrills availabl

179 fic, nonconserved NTE mutations in unrelated MND patients indicates NTE's importance in maintaining a

180 Therefore, the modified retroviral vector, MND, achieves higher net levels of expression due to a g

181 of the precursors and pathways through which MND is produced and evolves.

182 with FTD, nine with FTD and MND, and 23 with MND] and three carriers who had no clinical phenotype).

183 ith FTD, 12 with FTD and MND, and eight with MND]), and blood (47 patients [15 with FTD, nine with FT

184 = 72); and 4) familial and sporadic FTD with MND (n = 40).

185 of which were donated by people living with MND, family members and non-related controls, accompanie

186 with FTD, 11 with FTD and MND, and nine with MND]), cerebellum (40 patients [20 with FTD, 12 with FTD

187 Participants with MND were recruited through the Phenotype-Genotype-Biomar

188 ior increased over 4 months in patients with MND (right: 10.2%, 95% CI 2.0% to 18.4%, p=0.017; left:

189 probably coincidental, in some patients with MND a careful search for an underlying cancer is warrant

190 Twenty-nine patients with MND and 22 age-matched and gender-matched healthy contro

191 We have encountered 14 patients with MND and cancer who formed three distinct groups.

192 Patients with MND had 30% higher relative T2 muscle signal than contro

193 evious surveys showed that few patients with MND received NIV.

194 People with MND (pwMND) on the Scottish Clinical, Audit, Research an

195 ransplantation of stem cells transduced with MND-huWASp LV resulted in sustained, endogenous levels o

196 while 99.89% of the F9 cells transduced with MND-tNGFR-SN showed expression.

197 poradic and familial FTLD-U with and without MND and expand this disease spectrum to include reported

198 f familial and sporadic FTLD with or without MND.