ライフサイエンスコーパス: N-acetylaspartate

1 creases in striatal choline and decreases in N-acetylaspartate.

2 eatine, and NAAG was expressed as a ratio to N-acetylaspartate.

3 ipsilesional PMd myo-inositol and lower SMA N-acetylaspartate.

4 ine and creatine and lower concentrations of N-acetylaspartate.

5 myo-inositol (a marker of glial cells), and N-acetylaspartate (a marker of neuronal integrity).

6 The authors measured N-acetylaspartate (a putative neuronal marker) in the ri

7 The authors measured N-acetylaspartate (a putative neuronal marker), using in

8 t cancer cells, including elevated levels of N-acetylaspartate, a metabolite primarily associated wit

9 udy was to determine if the concentration of N-acetylaspartate, a neuronal and axonal marker, was low

10 Loss of N-acetylaspartate, a putative neuronal marker, from gray

11 Prefrontal N-acetylaspartate, an in vivo MRI measure related to syn

12 conclude that there is an early reduction in N-acetylaspartate and an increase in choline compounds i

13 tent was seen with weak associations between N-acetylaspartate and aspartate and glutamate and aspart

14 sonance spectroscopy studies have shown that N-acetylaspartate and choline-containing compounds can p

15 MRS voxels, suggesting that the hippocampal N-acetylaspartate and creatine alterations were not an a

16 trated significantly lower concentrations of N-acetylaspartate and creatine but normal choline concen

17 sed to measure the relative concentration of N-acetylaspartate and creatine, a marker of neural integ

18 There was no association between N-acetylaspartate and duration of illness or medication

19 There was no association between level of N-acetylaspartate and duration of illness or medication

20 Extracellular NAAG is hydrolyzed to N-acetylaspartate and glutamate by peptidase activity.

21 significant association between hippocampal N-acetylaspartate and glutamate content was seen with we

22 yl-L-aspartyl-L-glutamate (NAAG), to produce N-acetylaspartate and glutamate following the synaptic r

23 A reduction in the levels of N-acetylaspartate and glutamate, compared with total cre

24 yl-L-aspartyl-L-glutamate (NAAG) to liberate N-acetylaspartate and glutamate.

25 ptide N-acetyl-aspartylglutamate (NAAG) into N-acetylaspartate and glutamate.

26 individuals also showed greater decreases in N-acetylaspartate and in brain volume over 1 year of fol

27 gnetic resonance imaging and measurements of n-acetylaspartate and lactate using chemical shift magne

28 Right thalamic N-acetylaspartate and left thalamic N-acetylaspartate we

29 N-acetylaspartate and mI both had statistically signific

30 In transected adult nerves, N-acetylaspartate and N-acetyl aspartylglutamate decreas

31 The combination of N-acetylaspartate and N-acetylaspartyl glutamate (summed

32 to quantify gray matter volume (GMV) and the N-acetylaspartate and N-acetylaspartylglutamate/creatine

33 ect, quantitative link between a decrease in N-acetylaspartate and neuronal loss in a human neurodege

34 compared with sham tDCS, elevated prefrontal N-acetylaspartate and striatal glutamate + glutamine but

35 onger lasting effects of elevated prefrontal N-acetylaspartate and striatal glutamate + glutamine lev

36 artylglutamate (NAAG) to yield glutamate and N-acetylaspartate and that has been hypothesized to infl

37 xcitoxic glutamatergic process that leads to N-acetylaspartate and volume reductions.

38 with other brain metabolites (i.e., choline, N-acetylaspartate, and creatine).

39 metabolites: the exclusively neuronal/axonal N-acetylaspartate, and the predominantly glial creatine

40 spectroscopic ((1)H-MRS) imaging (to measure N-acetylaspartate as a marker of neuronal pathology) and

41 netic resonance spectroscopy measurements of N-acetylaspartate as an axon-specific monitor of central

42 sing left and right (1)H-MRS ratios(creatine/N-acetylaspartate) as input.

43 The neuronal compound N-acetylaspartate, as measured by magnetic resonance spe

44 levels of occipital cortex GABA, glutamate, N-acetylaspartate, aspartate, creatine, and choline-cont

45 The finding of reduced concentrations of N-acetylaspartate bilaterally suggests neuronal dysfunct

46 ne and phosphocreatine (Cho/Cr), and choline-N-acetylaspartate (Cho/NAA) ratios were obtained in the

47 N-Acetylaspartate, choline moieties, creatine-phosphocre

48 N-acetylaspartate, choline, and creatine in the right an

49 Concentrations of N-acetylaspartate, choline, and creatine were determined

50 Absolute levels of N-acetylaspartate, choline, myo-inositol, and creatine w

51 ique permits the simultaneous measurement of N-acetylaspartate, choline-containing compounds, creatin

52 Concentrations of N-acetylaspartate, choline-containing compounds, myo-ino

53 between the severity of head injury and the N-acetylaspartate/choline ratio.

54 Statistically significantly lower N-acetylaspartate/choline-containing metabolites (Cho) a

55 rain injury (DCBI) as assessed from relative N-acetylaspartate concentration (a marker of axonal inte

56 ant association between illness duration and N-acetylaspartate concentration in the right hippocampus

57 o a significant negative correlation between N-acetylaspartate concentration in the right hippocampus

58 rim assessments, mean normalized measures of N-acetylaspartate concentration tended to be higher in t

59 at female alcoholics had significantly lower N-acetylaspartate concentrations (-10.73%) relative to f

60 tine concentrations and delayed decreases in N-acetylaspartate concentrations.

61 We found significantly elevated creatine/N-acetylaspartate (Cr/NAA) unilaterally in 8 and bilater

62 Concentrations of N-acetylaspartate, creatine, and choline were determined

63 Levels of N-acetylaspartate, creatine, and choline were determined

64 Magnetic resonance spectroscopy measures of N-acetylaspartate-creatine and phosphocreatine (NAA/Cr),

65 in tissue (NABT), WM, GM and T2 lesions; and N-acetylaspartate/creatine (NAA/Cr) levels in WM.

66 magnetic resonance spectroscopic findings of N-acetylaspartate/creatine in frontal gray matter (r = -

67 e group exhibited a significant reduction of N-acetylaspartate/creatine levels in the right dorsolate

68 The lower N-acetylaspartate/creatine ratio in subjects with PTSD s

69 anxiety disorder patients had a 16.5% higher N-acetylaspartate/creatine ratio in the right dorsolater

70 The brain N-acetylaspartate/creatine ratio was reduced [patients (

71 associated with asymmetric increases in the N-acetylaspartate/creatine ratio, a suggested marker of

72 patients reporting childhood abuse had lower N-acetylaspartate/creatine ratios in the right dorsolate

73 N-Acetylaspartate/creatine resonance ratios were measure

74 At both the early and late time points the N:-acetylaspartate/creatine ratio (NAA/Cr) was significa

75 After transection at postnatal day 4, total N-acetylaspartate decreased by 80% (P14; p = 0.002) and

76 R spectroscopy marker of neuronal viability, N-acetylaspartate, did not differ between patients and c

77 e the signal peaks of choline, creatine, and N-acetylaspartate from fetal brain.

78 hose with GBM (which include lipid, alanine, N-acetylaspartate, gamma-aminobutyric acid, glutamine an

79 The hippocampal content of N-acetylaspartate, glutamate, GABA, glutamine, and aspar

80 mpal neuron loss and the cellular content of N-acetylaspartate, glutamate, GABA, glutamine, or aspart

81 c findings showed a significant reduction of N-acetylaspartate in all parts of the cerebellum, a sign

82 Here we provide the first evidence of N-acetylaspartate in breast cancer.

83 ylaspartate levels, and that 5 to 20% of the N-acetylaspartate in developing white matter is synthesi

84 temporal (p = 0.008) white matter; (2) lower N-acetylaspartate in frontal gray matter (p = 0.01); and

85 male alcoholics exhibited significantly less N-acetylaspartate in frontal gray matter relative to fem

86 isk factor for schizophrenia) on measures of N-acetylaspartate in healthy comparison subjects.

87 In contrast, N-acetylaspartate in other cortical regions and in compa

88 uced AN activation and lower neuronal marker N-acetylaspartate in prefrontal and parietal cortices.

89 Measures of N-acetylaspartate in the dorsolateral prefrontal cortex

90 explained by higher-than-expected levels of N-acetylaspartate in the healthy female comparison group

91 Relative levels of choline, creatine, and N-acetylaspartate in the left and right caudate, putamen

92 iminary study provides support for decreased N-acetylaspartate in the left frontal lobe in schizophre

93 a demonstrated significantly lower levels of N-acetylaspartate in the left frontal lobe.

94 tudies with schizophrenia show reductions in N-acetylaspartate in the medial temporal and prefrontal

95 h ALS also had significantly lower levels of N-acetylaspartate in the motor cortex (P < .01), subcort

96 naive patients with ALS had higher levels of N-acetylaspartate in the motor cortex than did riluzole-

97 aspartate antagonists has produced decreased N-acetylaspartate in the temporal cortex.

98 hite matter in all patients and reduction of N-acetylaspartate in the unaffected frontal white matter

99 N-acetylaspartate is a marker of neuronal health and num

100 e possibility has been raised, however, that N-acetylaspartate is expressed also by oligodendroglial

101 In AOA2, total N-acetylaspartate levels in the cerebellum strongly corr

102 hemispheres in both diseases by lower total N-acetylaspartate levels than controls.

103 Older subjects in both groups had lower N-acetylaspartate levels than the respective younger sub

104 Mean N-acetylaspartate levels were below those reported by in

105 dicate that neuronal adaptation can increase N-acetylaspartate levels, and that 5 to 20% of the N-ace

106 athology and decrease of the neuronal marker N-acetylaspartate measured by HRMAS 1HMRS.

107 c resonance imaging; brain concentrations of N-acetylaspartate, measured with proton magnetic resonan

108 etastatic potential, modulates glutamine and N-acetylaspartate metabolism in IBC cells in vitro, reve

109 related to neuronal and glial compartments: N-acetylaspartate, myo-inositol, and glutamate/glutamine

110 f glutamine (Gln), glutamate (Glu), Gln/Glu, N-acetylaspartate, myo-Inositol, lactate, and alanine.

111 Brain metabolites (N-acetylaspartate, myoinositol, choline, creatine) were

112 s had significantly higher concentrations of N-acetylaspartate, N-acetylaspartylglutamate, and aspart

113 for excitatory neurotransmission, including N-acetylaspartate, N-acetylaspartylglutamate, aspartate,

114 ltaneous measurement of compounds containing N-acetylaspartate (NA), choline (Cho), creatine-phosphoc

115 tio of choline-containing compounds [Cho] to N-acetylaspartate [NA] p< or =0.01) and right cerebellum

116 s ratios of different metabolite peak areas (N-acetylaspartate [NA]/creatine [Cr], NA/choline [Ch], a

117 images, and normalized the concentrations of N-acetylaspartate (NAA) and choline (Cho) in each ROI to

118 utcomes, P=.001) and with decreased absolute N-acetylaspartate (NAA) and choline concentrations in al

119 N-acetylaspartate (NAA) and creatine plus choline metabo

120 onstrated a significant relationship between N-acetylaspartate (NAA) and executive function.

121 opeptide N-acetylaspartylglutamate (NAAG) to N-acetylaspartate (NAA) and glutamate (G).

122 ion into white or gray brain matter based on N-acetylaspartate (NAA) and on membrane-derived complex

123 netic resonance spectroscopic measurement of N-acetylaspartate (NAA) and other metabolites, together

124 he brain to observe natural 13C abundance of N-acetylaspartate (NAA) and the appearance of 13C-labele

125 We found that atrophy-corrected hippocampal N-acetylaspartate (NAA) concentration was lower in cogni

126 Three days following seizure activity, N-acetylaspartate (NAA) declined and lactate increased i

127 It is unclear whether N-acetylaspartate (NAA) depletions documented in schizop

128 ansferase 8-like) catalyzes the formation of N-acetylaspartate (NAA) from acetyl-CoA and aspartate.

129 hod involves: (a) chemical synthesis of [14C]N-acetylaspartate (NAA) from L-[14C]Asp; (b) use of [14C

130 ASPA acts to hydrolyze N-acetylaspartate (NAA) into l-aspartate and acetate, bu

131 N-acetylaspartate (NAA) is a concentrated, neuron-specif

132 N-Acetylaspartate (NAA) is one of the most abundant amin

133 N-acetylaspartate (NAA) is present at very high concentr

134 e spectroscopy (MRS) studies have shown that N-acetylaspartate (NAA) is reduced not only in the ipsil

135 Baseline N-acetylaspartate (NAA) level, myo-inositol (mI) in norm

136 Absolute N-acetylaspartate (NAA) levels from the DLPFC were signi

137 Transient changes in N-acetylaspartate (NAA) levels were sometimes found in a

138 decades have indicated that biosynthesis of N-acetylaspartate (NAA) occurs primarily in the mitochon

139 (rCBV) represented elevated choline (Cho)-to-N-acetylaspartate (NAA) ratio (hereafter, Cho/NAA ratio)

140 ellular and extract data have suggested that N-acetylaspartate (NAA) reflects neuronal mitochondrial

141 talyzes the hydrolysis of neuronally derived N-acetylaspartate (NAA) to acetate and aspartic acid.

142 ubjects showed significantly lower ratios of N-acetylaspartate (NAA) to choline-containing compounds

143 The ratio of N-acetylaspartate (NAA) to creatine (Cr) was derived fro

144 SPA; EC 3.5.1.15) catalyzes deacetylation of N-acetylaspartate (NAA) to generate free acetate in the

145 study, diffusion of the neuronal metabolite N-acetylaspartate (NAA) was measured in the human normal

146 trast, the apparent diffusion coefficient of N-acetylaspartate (NAA) was significantly elevated, sugg

147 te maps of creatine (Cr), choline (Cho), and N-acetylaspartate (NAA) were segmented into 81 regions w

148 D (i.e. increased myo-inositol and decreased N-acetylaspartate (NAA)).

149 study used MRS to examine concentrations of N-acetylaspartate (NAA), a marker of neuronal integrity

150 Studies indicate that N-acetylaspartate (NAA), a marker of neuronal integrity,

151 N-acetylaspartate (NAA), an indicator of neuronal mitoch

152 to assess glutamate (Glu), glutamine (Gln), N-acetylaspartate (NAA), and choline (Cho) levels in the

153 pectroscopy, we found lower brain glutamate, N-acetylaspartate (NAA), and creatine concentrations in

154 stribution of the metabolites choline (Cho), N-acetylaspartate (NAA), and creatine were calculated in

155 of the energy state (ATP, ATP-catabolites), N-acetylaspartate (NAA), antioxidant defenses (ascorbic

156 ain Glu on neuroaxonal integrity measured by N-acetylaspartate (NAA), brain volume, and clinical outc

157 We examined the relationships between N-acetylaspartate (NAA), choline (Cho) and creatine (Cr)

158 Distributions of N-acetylaspartate (NAA), choline (Cho), and creatine (Cr

159 Concentrations of N-acetylaspartate (NAA), choline (Cho), creatine (Cr), m

160 Absolute N-acetylaspartate (NAA), choline, and creatine levels we

161 Quantitative measures of N-acetylaspartate (NAA), choline, and creatine values an

162 solute concentrations of neurometabolite for N-acetylaspartate (NAA), choline, creatine, and lactate

163 e) nonsmokers (n = 30) and smokers (n = 35), N-acetylaspartate (NAA), choline-containing compounds, c

164 Absolute N-acetylaspartate (NAA), creatine (Cr), and choline (Cho

165 examined with H-1 MR spectroscopy to measure N-acetylaspartate (NAA), creatine (Cr), and choline (Cho

166 y to measure absolute rostral and caudal ACC N-acetylaspartate (NAA), creatine (Cr), and choline (Cho

167 terials and Methods: The T2 distributions of N-acetylaspartate (NAA), creatine (Cr), and choline (Cho

168 We measured concentrations and ratios of N-acetylaspartate (NAA), creatine and phosphocreatine (C

169 N-Acetylaspartate (NAA), creatine, choline, total glutam

170 tients displayed some combination of reduced N-acetylaspartate (NAA), enhanced glutamate/glutamine (G

171 We found that N-acetylaspartate (NAA), glutamate and glutathione were

172 Cerebellar concentrations of N-acetylaspartate (NAA), myo-inositol, and glutamate as

173 nd phosphocreatine, glutamine and glutamate, N-acetylaspartate (NAA), myo-inositol, and lactate.

174 phocreatine/EPP (both p < 0.05); for lactate/N-acetylaspartate (NAA), only xenon-augmented hypothermi

175 resonance spectroscopy to measure prefrontal N-acetylaspartate (NAA), which is mainly localized in ne

176 y in aspartoacylase (ASPA), which hydrolyzes N-acetylaspartate (NAA).

177 breaks, Scans 1-2) with thalamic volumes and N-acetylaspartate (NAA)/choline (Cho), and fractional an

178 In FGR pregnancies, a reduction in N-acetylaspartate (NAA)/choline ratio and detection of l

179 ophy scores and single voxel (basal ganglia) N-acetylaspartate (NAA)/Choline, NAA/Creatine and myo-in

180 nd a loss of correlation between hippocampal N-acetylaspartate (NAA)/Cr and Glx/Cr in patients with s

181 Average N-acetylaspartate (NAA)/creatine-phosphocreatine (Cr) an

182 oscopic imaging (MRSI) measurements of brain N:-acetylaspartate (NAA), a marker of axonal integrity,

183 metric, metabolite maps (choline, creatine, N-acetylaspartate [NAA], and/or citrate), and statistica

184 xel, 20-msec-echo-time MR spectra (including N-acetylaspartate [NAA], choline [Ch], creatine and phos

185 vo measure of prefrontal neuronal pathology (N:-acetylaspartate [NAA] levels) in patients with schizo

186 myelin content and DTS to study metabolite (N-acetylaspartate, NAA) diffusion within axons in patien

187 ies of N-acetyl-containing compounds (mainly N-acetylaspartate, NAA), choline-containing compounds (C

188 otropy (FA)) and axonal dysfunction (reduced N-acetylaspartate NAAc).

189 ampal atrophy, hypometabolism, and decreased N-acetylaspartate, often attributed to neuron loss and g

190 nce spectroscopy to assess concentrations of N-acetylaspartate, often considered a marker of neuronal

191 induce differences in glutamate + glutamine, N-acetylaspartate, or gamma-aminobutyric acid levels in

192 ortex thalamus, and cerebellum may also have N-acetylaspartate reductions.

193 In order to investigate N-acetylaspartate specificity for white matter axons, tr

194 correlated with: (1) lower concentrations of N-acetylaspartate (spectroscopic marker of neuronal viab

195 trated significantly lower concentrations of N-acetylaspartate than the comparison subjects in both t

196 Measured concentrations of putaminal total N-acetylaspartate (tNAA) (8.1 +/- 0.2 vs 9.4 +/- 0.4; P

197 isease had a decrease of 10% in the ratio of N-acetylaspartate to choline (P=0.003), an increase of 2

198 We calculated the ratio of N-acetylaspartate to choline (which increases with brain

199 We calculated N-acetylaspartate to choline ratios (NAA/choline), lacta

200 proton magnetic resonance spectroscopy (MRS; N-acetylaspartate to creatine (NAA/Cr) ratios)-derived h

201 The marked difference in the distribution of N-acetylaspartate to creatine between PPA and Alzheimer'

202 a statistically significant decrease in the N-acetylaspartate to creatine ratio in gray matter compa

203 In the PPA group, there was an asymmetrical N-acetylaspartate to creatine ratio reduction compared w

204 The ratio of N-acetylaspartate to creatine was significantly lower in

205 eurofilament light chain (NFL), the ratio of N-acetylaspartate to creatinine levels (a magnetic reson

206 = 0.555 and P < .001) and with the ratio of N-acetylaspartate to creatinine levels in parietal gray

207 The N-acetylaspartate-to-creatine (NAA/Cr) ratio, which refl

208 Decreases in N-acetylaspartate-to-creatine ratio, an index of neurona

209 ongest association observed was that between N-acetylaspartate-to-myo-inositol ratio and Braak stage

210 The N-acetylaspartate-to-myo-inositol ratio proved to be the

211 Total N-acetylaspartate, total creatine and total choline diff

212 mediated process that may explain decreased N-acetylaspartate, volume loss, and the poor outcomes of

213 At 24 days posttransection, N-acetylaspartate was increased (42%; p = 0.02) in nontr

214 Ipsilesional N-acetylaspartate was significantly related to proximal

215 thalamic N-acetylaspartate and left thalamic N-acetylaspartate were significantly correlated in the p

216 frontal lobe white matter concentrations of N-acetylaspartate were significantly lower (-8.8%) than

217 Lower concentrations of white matter N-acetylaspartate, which may indicate neuronal loss or d