ライフサイエンスコーパス: N-acetylaspartate

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

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

3 natomical volume, fractional anisotropy, and N-acetylaspartate.

4 magnetic resonance spectroscopy measures of N-acetylaspartate.

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

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

7 .93 and 0.93 for creatine, 0.93 and 0.93 for N-acetylaspartate, 0.80 and 0.72 for myo-inositol, and 0

8 e and branched chain amino acids, generating N-acetylaspartate; (2) the alanine-generating Cahill-cyc

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

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

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

12 Consistently, reduced N-acetylaspartate, a marker of neuronal viability, was o

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

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

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

16 l reversals of taurine, glutamine, and total N-acetylaspartate across both regions.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

33 scan, we simultaneously obtained 3D maps of N-acetylaspartate and lactate at a nominal spatial resol

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

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

36 N-acetylaspartate and mI both had statistically signific

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

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

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

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

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

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

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

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

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

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

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

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

49 late levels of the neuronal viability marker N-acetylaspartate as measured with in vivo proton magnet

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

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

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

53 N-acetylaspartate availability is essential for juvenile

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

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

56 N-Acetylaspartate, choline moieties, creatine-phosphocre

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

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

59 asure cerebral neurochemical concentrations (N-acetylaspartate, choline, glutamate, glutamine, myo-in

60 Glx (as well as N-acetylaspartate, choline, myo-inositol and creatine) g

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

79 ) = -0.17, beta-(right) = -0.15, ps = .002), N-acetylaspartate/creatine ratio (beta-(left)= -0.40, be

80 ifferences were greater at younger ages, and N-acetylaspartate/creatine ratio differences were greate

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

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

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

84 RI), proton magnetic resonance spectroscopy (N-acetylaspartate/creatine ratio), and functional MRI ac

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

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

87 N-Acetylaspartate/creatine resonance ratios were measure

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

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

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

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

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

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

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

95 igodendrocyte abnormalities, decreased total N-acetylaspartate highlights neuronal health disturbance

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

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

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

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

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

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

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

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

104 Measures of N-acetylaspartate in the dorsolateral prefrontal cortex

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

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

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

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

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

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

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

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

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

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

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

116 vity correlated with total choline and total N-acetylaspartate levels early in disease.

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

118 accompanying lower and increasingly abnormal N-acetylaspartate levels relative to those of typically

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

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

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

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

123 rial oxidative stress, and maintains ATP and N-acetylaspartate levels, resulting in attenuated infarc

124 No group effect was found in measures of N-acetylaspartate levels.

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

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

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

128 F in the ASD group correlated inversely with N-acetylaspartate metabolite levels throughout the front

129 r findings and the correlations of rCBF with N-acetylaspartate metabolite levels.

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

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

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

133 N-acetyl compounds (N-acetylaspartate + N-acetylaspartylglutamate), glutamat

134 glutamatergic metabolites, myo-inositol, and N-acetylaspartate+N-acetylaspartylglutamate (tNAA) in th

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

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

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

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

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

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

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

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

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

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

145 ine (tCr), choline (Cho), myo-inositol (mI), N-acetylaspartate (NAA) and glutamate/glutamine (Glx) we

146 dy found BD subjects to have lower levels of N-acetylaspartate (NAA) and glycerophosphocholine plus p

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

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

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

150 analysis could not be done because thalamic N-acetylaspartate (NAA) concentration alone accurately p

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

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

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

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

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

156 coefficients (ADC) of choline, creatine, and N-acetylaspartate (NAA) in two brain regions: the thalam

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

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

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

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

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

162 N-acetylaspartate (NAA) is synthesized by aspartate N-ac

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

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

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

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

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

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

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

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

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

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

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

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

175 with and without reduced signal intensity of N-acetylaspartate (NAA) was visible on metabolic images

176 In the brain, glutamate, serine, and N-acetylaspartate (NAA) were reduced after LPS, whereas

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

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

179 We hypothesize that white matter levels of N-acetylaspartate (NAA), a chemical involved in the meta

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

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

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

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

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

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

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

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

188 culate absolute metabolite concentrations of N-acetylaspartate (NAA), choline (Cho) and creatine (Cr)

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

204 N-acetylaspartate (NAA), glutamate, creatine, choline, m

205 ically significant decrease in the levels of N-acetylaspartate (NAA), myo-inositol (mI), scyllo-inosi

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

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

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

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

210 cell 4 to 6 carbon dicarboxylates as well as N-acetylaspartate (NAA).

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

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

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

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

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

216 bolite concentrations as ratios to creatine (N-acetylaspartate (NAA)/creatine (Cr) and choline (Cho)/

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

218 Reduced N-acetylaspartate (NAA)/total creatine (tCr) ratio found

219 ignificantly decreased the medial prefrontal N-acetylaspartate (NAA; p = 0.043) and glutamate-glutami

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

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

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

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

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

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

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

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

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

229 3)(-), together with citrate, aspartate, and N-acetylaspartate on human prostate cancer tissues.

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

231 Both lactate (P < 0.0001) and N-acetylaspartate (P < 0.001) differed between infarcted

232 lude small metabolites such as adenosine and N-acetylaspartate previously associated with astrocytes

233 e increase in glutamate + glutamine to total N-acetylaspartate ratio during ketamine infusion compare

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

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

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

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

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

239 ontaining metabolites (tCho) and lower total N-acetylaspartate (tNAA) were associated with higher ora

240 Concentrations of total N-acetylaspartate (tNAA), myo-inositol (mI), total choli

241 and wild-type gliomas (eg, tumoral Glu/total N-acetylaspartate [tNAA], P = .0054), oligodendroglioma

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

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

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

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

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

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

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

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

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

251 = 0.555 and P < .001) and with the ratio of N-acetylaspartate to creatinine levels in parietal gray

252 Motor cortex total N-acetylaspartate to myo-inositol ratio (tNAA:mIns) sign

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

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

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

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

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

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

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

260 Ipsilesional N-acetylaspartate was significantly related to proximal

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

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

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