ライフサイエンスコーパス: hypometabolism

1 ) and tissue failure, apoptosis, or atrophy (hypometabolism).

2 twork, but not with brain atrophy or glucose hypometabolism.

3 and fat mass before LTx was associated with hypometabolism.

4 + 3), defined as hippocampal atrophy or FDG hypometabolism.

5 exhibits mild obesity without hyperphagia or hypometabolism.

6 t significantly related to either atrophy or hypometabolism.

7 al activity is reflected by cortical glucose hypometabolism.

8 pection and presented in previous reports of hypometabolism.

9 ecuneus), strongly overlapping with regional hypometabolism.

10 th IDU, resulting in more extensive cortical hypometabolism.

11 c cytochrome oxidase contributions to energy hypometabolism.

12 ellar hypometabolism and 13% had ipsilateral hypometabolism.

13 lism, whereas 15% had ipsilateral cerebellar hypometabolism.

14 ed isolated bilateral anterior temporal lobe hypometabolism.

15 more restricted distribution than an area of hypometabolism.

16 were associated with ipsilateral cerebellar hypometabolism.

17 were associated with ipsilateral cerebellar hypometabolism.

18 me in the presence of bilateral temporal PET hypometabolism.

19 rovement of clinical symptoms and cerebellar hypometabolism.

20 a deposition and Alzheimer's disease-related hypometabolism.

21 uced hippocampal volume, and greater FDG-PET hypometabolism.

22 rocytes are the key target in 5'-AMP induced hypometabolism.

23 ending the larval development period through hypometabolism.

24 n has little to no association with regional hypometabolism.

25 sed cerebral amyloid deposition and cerebral hypometabolism.

26 true, we would expect wide-spread, cortical hypometabolism.

27 eimer's disease (AD), amyloid deposition and hypometabolism.

28 rmal; 20.6% diabetic individuals), (18)F-FDG hypometabolism ((18)F-FDG ratio < 1.31) in the AD signat

29 induced ipsilateral neostriatal and thalamic hypometabolism 3-day post-injury, with subsequent metabo

30 y posterior cingulate cortex and hippocampal hypometabolism (81%), whereas neocortical abnormalities

31 attern other than bilateral temporo-parietal hypometabolism, a cause of dementia other than AD should

32 Finally, before hypometabolism, a hypermetabolic phase was identified fo

33 ing connectivity abnormalities; furthermore, hypometabolism, Abeta plaque accumulation, reduction of

34 y associated with REE or hypermetabolism and hypometabolism after LTx.

35 abolic pattern of bilateral temporo-parietal hypometabolism allows differentiation between other dege

36 ere associated with contralateral cerebellar hypometabolism and 13% had ipsilateral hypometabolism.

37 ere associated with contralateral cerebellar hypometabolism and 19% were associated with ipsilateral

38 e focal lesions had contralateral cerebellar hypometabolism and 27% had ipsilateral cerebellar hypome

39 Schizophrenia is frequently accompanied by hypometabolism and altered gene expression in the prefro

40 predicts the regional anatomic expansion of hypometabolism and atrophy in persons with mild cognitiv

41 INTERPRETATION: Although both hypometabolism and beta-amyloid (Abeta) deposition are d

42 s, AD patients showed typical patterns of BL hypometabolism and BL amyloid deposition, with a similar

43 The spatial overlap between hypometabolism and disruption of connectivity in cortica

44 To investigate the association between brain hypometabolism and hypermetabolism with motor scores of

45 were performed for regions with significant hypometabolism and hypermetabolism.

46 In conclusion, hypometabolism and hypothermia in endotoxic shock are no

47 Cerebral hypometabolism and impaired episodic memory were observe

48 phic features, patterns of brain atrophy and hypometabolism and longitudinal clinical trajectories of

49 position was predominant, together with high hypometabolism and lower but still significant atrophy;

50 lline an interesting candidate to combat the hypometabolism and neuronal dysfunction associated with

51 One emerging link between glucose hypometabolism and progression of AD is the nutrient-res

52 evidence that tau is more closely linked to hypometabolism and symptomatology than amyloid.

53 time, in normal elderly its link to AD-like hypometabolism and to AD-like memory decline.

54 ft MTL in AD at 2 different levels: regional hypometabolism and verbal memory.

55 TD is most robustly associated with atrophy, hypometabolism and/or hypoperfusion in the dorsolateral

56 ficant differences in the levels of atrophy, hypometabolism, and Abeta deposition were found in most

57 rarchy and relationships between Abeta load, hypometabolism, and atrophy.

58 Gray matter atrophy, glucose hypometabolism, and beta-amyloid Abeta deposition are we

59 al relationships between amyloid deposition, hypometabolism, and cognition, and (2) associations betw

60 psy is characterized by hippocampal atrophy, hypometabolism, and decreased N-acetylaspartate, often a

61 89 years) who were negative for amyloidosis, hypometabolism, and hippocampal atrophy.

62 ely hippocampal volume loss, temporoparietal hypometabolism, and neocortical beta-amyloid (Abeta) dep

63 Instead, cortical hypometabolism appears to be linked to global amyloid bu

64 However, it is well known that atrophy and hypometabolism are prominent in different anatomical are

65 esent study is to compare brain atrophy with hypometabolism as preclinical markers of Alzheimer's dis

66 esence of classic bilateral temporo-parietal hypometabolism as seen in Alzheimer's type dementia.

67 Longitudinal regional expansion of cerebral hypometabolism, as a measure of neuronal dysfunction in

68 FTLD patients with right superior aTL hypometabolism, as determined on individual ROI analyses

69 g impression that bilateral temporo-parietal hypometabolism, as noted on FDG PET imaging, is the meta

70 significance of the shift from MTL hyper- to hypometabolism associated with IR.

71 retention and low hippocampal volume or FDG hypometabolism at baseline (preclinical AD stages 2 + 3)

72 Amyloid deposition was more extended than hypometabolism at BL and showed only minor changes over

73 erate and later stages of disease (LMCI/AD), hypometabolism becomes more pronounced and more closely

74 ostic accuracy of bilateral temporo-parietal hypometabolism being associated with AD were 93%, 63%, a

75 on brain (18)F-FDG PET/CT imaging was lobar hypometabolism, being observed in 21 of 23 (91.3%) patie

76 ttern characterized by caudate and putamenal hypometabolism but also included mediotemporal metabolic

77 Entorhinal tau was associated with frontal hypometabolism, but this dysfunction was not associated

78 Detection of cortical or subcortical hypometabolism by 18F-FDG PET is an unfavorable predicto

79 escribe the relationship between atrophy and hypometabolism by means of a data-driven statistical mod

80 ients with Alzheimer disease (AD), prominent hypometabolism can occur in brain regions without major

81 regions accounts for the posterior cingulate hypometabolism commonly detected in positron emission to

82 ve deficits and greater cortical atrophy and hypometabolism compared to late-onset patients at a simi

83 l amyloid burden and greater medial temporal hypometabolism compared with matched ApoE4- patients.

84 reas (18)F-FDG PET demonstrated mesiofrontal hypometabolism consistent with the clinical diagnosis of

85 se metabolism PET showed multifocal cortical hypometabolism corresponding to the locations of tubers

86 on to age-associated overweight and includes hypometabolism, enhanced skin vasoconstriction, decrease

87 Hypometabolism extended over wider regions than hypoperf

88 shold mean FDG values were considered as FDG hypometabolism [FDG+]).

89 hypoperfusion that overlap considerably with hypometabolism frequently reported with FDG PET.

90 However, acute hypometabolism has long been described in small mammals

91 rognostic importance of PET-identified focal hypometabolism; however, 2 investigations indicated that

92 the patients and with ipsilateral cerebellar hypometabolism in 21% of the patients.

93 ere associated with contralateral cerebellar hypometabolism in 38% of the patients and with ipsilater

94 [18F]fluorodeoxyglucose revealed widespread hypometabolism in a pattern found in sporadic multiple s

95 ceptor-deficient mice undergo 5'-AMP-induced hypometabolism in a similar fashion.

96 es to characterize the AD-related pattern of hypometabolism in a single measurement.

97 icted hypermetabolism in MCI-progressors and hypometabolism in AD in medial temporal regions.

98 These data suggest that the observed hypometabolism in AD may contribute to its deposition of

99 nondiabetic individuals may enhance glucose hypometabolism in AD signature regions.

100 iomarkers, such as (18)F-FDG PET evidence of hypometabolism in AD-affected brain regions.

101 at severity of delusions was associated with hypometabolism in additional prefrontal and anterior cin

102 PET revealed parieto-temporal hypometabolism in all individuals scanned.

103 These data suggest that hypometabolism in Alzheimer's disease is related to redu

104 ed to symptomatology and patterns of glucose hypometabolism in Alzheimer's disease, in contrast to th

105 ined by abnormally low hippocampal volume or hypometabolism in an Alzheimer disease-like pattern on 1

106 tient groups, ApoE4+ subjects showed greater hypometabolism in bilateral medial temporal and right la

107 cantly contribute to longitudinally evolving hypometabolism in brain regions not strongly affected by

108 es a plausible mechanistic rationale for the hypometabolism in brain that precedes AD diagnosis and s

109 The induction of hypometabolism in cells and organs to reduce ischemia da

110 A1c was associated with greater AD signature hypometabolism in cognitively normal subjects (OR, 1.93;

111 regions, and ApoE4- patients showed greater hypometabolism in cortical areas, including supplementar

112 s associated with greater posterior cortical hypometabolism in early-onset Alzheimer's disease.

113 sitron emission tomography imaging confirmed hypometabolism in extra-cerebellar regions such as the b

114 ogy to induce a safe and reversible state of hypometabolism in humans, unlocking many applications ra

115 NI attenuated hypoxia-induced hypothermia or hypometabolism in lean rats, but not in obese rats.

116 ed by PPA subtype, with left temporoparietal hypometabolism in LPA, left frontal hypometabolism in PN

117 s of MC4R is known to induce hyperphagia and hypometabolism in mice.

118 showed perirolandic and variable prefrontal hypometabolism in most patients.

119 Anosognosia in AD patients correlated with hypometabolism in orbitofrontal (OFC) and posterior cing

120 parietal hypometabolism in LPA, left frontal hypometabolism in PNFA, and left anterior temporal hypom

121 tabolism in PNFA, and left anterior temporal hypometabolism in SD.

122 Compared with controls, the patients showed hypometabolism in several regions that, most notably, in

123 se who declined showed memory impairment and hypometabolism in temporal lobe neocortex and Hip.

124 r's and autism patients had relative glucose hypometabolism in the anterior and posterior cingulate a

125 ation with semantic impairment was degree of hypometabolism in the anterior fusiform region subjacent

126 There was mild hypometabolism in the caudate nucleus (-8.4% vs. control

127 ability mapping revealed additional areas of hypometabolism in the cingulate gyrus.

128 However, DLB showed greater hypometabolism in the medial occipital lobe, orbitofront

129 ial temporal lobe volume and greater glucose hypometabolism in the medial temporal lobe compared with

130 There was definite frontotemporal hypometabolism in the MRI-abnormal group (particularly i

131 nt study to investigate the possible role of hypometabolism in the pathogenesis of AD.

132 As hypometabolism in the patients' rostral fusiform was eve

133 Hypometabolism in the posterior parietal cortex (PPC) is

134 hypothesis is consistent with the selective hypometabolism in the posteromedial cortex reported in a

135 Extensive hypometabolism in the prefrontal or anterior temporal ar

136 nhibition') and demonstrated more pronounced hypometabolism in the right superior aTL, the left tempo

137 regional patterns of amyloid deposition and hypometabolism in the same population of mild AD subject

138 ion tomography (PET) consisting of bilateral hypometabolism in the temporal lobes.

139 There was no significant hypometabolism in the temporal or frontal lobes.

140 ive if they displayed the classic pattern of hypometabolism in the temporoparietal regions.

141 h C9orf72-positive ALS had discrete relative hypometabolism in the thalamus and posterior cingulate c

142 postoperative seizures of any frequency had hypometabolism in the thalamus contralateral to that of

143 lucose (FDG-PET) shows different patterns of hypometabolism in these disorders that might aid differe

144 ke was significant asymmetric (favoring left hypometabolism) in PPA (p < 0.005) but not in AD.

145 Areas of relative hypometabolism included the left superior medial gyrus,

146 PCA and DLB showed overlapping patterns of hypometabolism involving the lateral occipital lobe, lin

147 : PCA and DLB showed overlapping patterns of hypometabolism involving the lateral occipital lobe, lin

148 Patients with thalamic hypometabolism ipsilateral to the removed temporal lobe

149 Regional glucose hypometabolism is a defining feature of Alzheimer diseas

150 roups suggest that the mitochondrion-centred hypometabolism is a key feature of ageing brains and Alz

151 Occipital hypometabolism is a potential antemortem marker to disti

152 Glucose hypometabolism is a prominent feature of the brains of p

153 Mild Cognitive Impairment (MCI) and glucose hypometabolism is an early pathological change within AD

154 Striatal hypometabolism is associated with clinical disease sever

155 We hypothesized 1) that lateral PPC hypometabolism is associated with impaired spatial atten

156 Brain hypometabolism is associated with the clinical consequen

157 udy confirms that bilateral temporo-parietal hypometabolism is indeed the classic metabolic abnormali

158 Here, we show how a state of hypometabolism is initiated by 5'-AMP uptake by erythroc

159 ta accumulation, Alzheimer's disease-related hypometabolism is more specific to brain regions showing

160 r investigations reveal that 5'-AMP mediated hypometabolism is probably triggered by reduced oxygen t

161 olic rate and enter a condition of regulated hypometabolism known as torpor.

162 baseline and longitudinally) and with brain hypometabolism (longitudinally).

163 wn to lead to specific patterns of (18)F-FDG hypometabolism, mainly in superficial brain structures,

164 lation occurs in AD, suggesting that glucose hypometabolism may impair the protective roles of O-GlcN

165 at disruption of functional connectivity and hypometabolism may represent early functional consequenc

166 Progressive E4-related hypometabolism may underlie the known increased suscepti

167 -Pittsburgh compound B ((11)C-PiB) and brain hypometabolism measured using (18)F-FDG PET.

168 ed with magnetic resonance imaging (MRI) and hypometabolism measured with positron emission tomograph

169 nal imaging studies suggest that patterns of hypometabolism (measured by [(18)F] fluorodeoxyglucose p

170 y resting-state fMRI, even in the absence of hypometabolism (measured with PET [(18)F]FDG) or detecta

171 on, and (2) associations between amyloid and hypometabolism measurements and longitudinal cognitive m

172 n of equally thresholded statistical T maps (hypometabolism minus amyloid burden), resulting from vox

173 Cerebral hypometabolism, mitochondrial dysfunction, and beta-amyl

174 cal AD group on measures of FDG PET regional hypometabolism, MR regional brain volume loss, cerebrova

175 ic response to injury, and that the relative hypometabolism observed following ASP may be a reflectio

176 ron emission tomography scans revealed focal hypometabolism of superior lateral premotor cortex and s

177 e evidence that in very early AD, asymmetric hypometabolism of the lateral PPC causes spatial attenti

178 trophy on structural MR imaging, patterns of hypometabolism on (18)F-FDG PET, and detection of cerebr

179 ave both been associated with occipital lobe hypometabolism on (18)F-FDG PET, whereas relative sparin

180 Clinical variables, atrophy on MRI, hypometabolism on 18F-fluorodeoxyglucose positron emissi

181 disease (AD) is characterized by progressive hypometabolism on [(18)F]-fluorodeoxyglucose positron em

182 It was associated with left-sided frontal hypometabolism on FDG-PET imaging (Individual II) and wi

183 closely matches the established patterns of hypometabolism on fluorine 18 fluorodeoxyglucose (FDG) p

184 and had predominant right-sided atrophy and hypometabolism on magnetic resonance imaging and 18-fluo

185 with infantile spasms and bitemporal glucose hypometabolism on PET comprise a relatively homogeneous

186 These hypometabolism-only (HO) areas may not be explained easi

187 stem was used to assess the degree of either hypometabolism or amyloid binding in specified regions.

188 nts) revealed parieto-occipital dysfunction (hypometabolism or hypoperfusion) in all 7 tested patient

189 We aimed to determine whether patterns of hypometabolism or the cingulate island sign differed bet

190 orodeoxyglucose positron emission tomography hypometabolism, or both).

191 Regional hypometabolism overlaps to a large degree between PCA an

192 Conclusion: Regional hypometabolism overlaps to a large degree between PCA an

193 ibited a spatial pattern of cerebral glucose hypometabolism (P < 0.001) involving the occipital lobes

194 ibited a spatial pattern of cerebral glucose hypometabolism (P < 0.001) involving the occipital lobes

195 By 6 days post-contusion, the hypometabolism partially reversed in all structures.

196 ly derived regions of interest reflecting AD hypometabolism pattern (metaROI)--to distinguish moderat

197 We hypothesized that hypometabolism patterns would differ across variants, re

198 In these patients, occipital hypometabolism preceded some clinical features of DLB.

199 er's disease that is independent of neuronal hypometabolism, predates changes in brain perfusion, exa

200 The FDG-positive subgroup showed only hypometabolism, predominantly in AD-sensitive areas exte

201 Hypometabolism progressed over time in almost all subjec

202 the notion that glucose hypermetabolism and hypometabolism reflect fundamentally different aspects o

203 In contrast, frontal hypometabolism related to the common age-related entorhi

204 In contrast, similar patterns of hypometabolism relative to controls were found in both p

205 uroectodermal tumor (PNET) demonstrated mild hypometabolism relative to cortical gray matter.

206 Insula hypometabolism (relative to whole-brain mean) was associ

207 Neuroimaging studies have shown hypometabolism (representing impending cell failure) and

208 ing to assess amyloid accumulation and brain hypometabolism, respectively.

209 myloid-negative cases had subtle atrophy and hypometabolism, restricted to the retrosplenial/posterio

210 se findings suggest that cortical areas with hypometabolism should be interpreted as regions mostly n

211 Atrophy and hypometabolism significantly correlated in the hippocamp

212 se stages show overlapping brain atrophy and hypometabolism spread in temporal, parietal and cortical

213 odification and associated neuronal loss and hypometabolism start in the entorhinal cortex (EC) in ea

214 ted by significant improvement of cerebellar hypometabolism (statistical parametric mapping analyses,

215 of hippocampal memory linked to hippocampal hypometabolism, suggesting the possibility that brain Gl

216 cases usually showed patterns of atrophy and hypometabolism suggestive of another degenerative disord

217 er cases with normal structural imaging have hypometabolism suggestive of underlying neurodegeneratio

218 , and PCA showed more asymmetric patterns of hypometabolism than DLB.

219 ted prodromal AD patients showed more severe hypometabolism than poorly educated prodromal AD patient

220 peculiar spatial pattern of cerebral glucose hypometabolism that was most marked in MMF patients with

221 peculiar spatial pattern of cerebral glucose hypometabolism that was most marked in MMF patients with

222 I with nonmemory deficits ranged from absent hypometabolism to FTD and DLB PET patterns.

223 eview how O-GlcNAc may link cerebral glucose hypometabolism to progression of AD and summarize data r

224 etabolism and 27% had ipsilateral cerebellar hypometabolism to the most severe focal injury.

225 Early ictal hypometabolism, transient decreases in cell swelling and

226 Regional hypometabolism was assessed compared with a control coho

227 Prefrontal hypometabolism was associated with reduced clinical func

228 erior frontal and supplementary motor cortex hypometabolism was common to both patient groups, and th

229 tio (OR) for abnormal AD signature (18)F-FDG hypometabolism was elevated (2.28; 95% confidence interv

230 t of diminished cortical uptake, more severe hypometabolism was found in the mesial temporal regions

231 Parietal hypometabolism was greater in lvPPA-high than lvPPA-low.

232 The cortical hypometabolism was more extensive in HIV-1-infected subj

233 predictions and with models of CR, cerebral hypometabolism was more severe in the group of bilingual

234 Hypometabolism was most commonly observed in the parieta

235 Greater Alzheimer's disease-related hypometabolism was observed in brain regions that showed

236 over time, whereas significant expansion of hypometabolism was observed, almost exclusively within a

237 Extensive frontotemporal hypometabolism was predictive for a lower survival using

238 In summary, temporoparietal cortical hypometabolism was seen in non-demented Parkinson's dise

239 In statistical parametric mapping, striatal hypometabolism was significantly correlated with the sev

240 Subtle connectivity disruptions and hypometabolism were already present in amyloid-positive

241 Patterns of hypometabolism were assessed at the single subject-level

242 abolic pattern of bilateral temporo-parietal hypometabolism were determined using pathologic diagnosi

243 Hypermetabolism/hypometabolism were low but present at the end of the st

244 ere associated with contralateral cerebellar hypometabolism, whereas 15% had ipsilateral cerebellar h

245 ns: (1) in the hippocampus, atrophy exceeded hypometabolism, whereas Abeta load was minimal; (2) in p

246 ere associated with contralateral cerebellar hypometabolism, whereas only 8% were associated with ips

247 apping temporal atrophy and temporo-parietal hypometabolism, while the later disease stages show over

248 Thus, increased similarity of FU hypometabolism with BL amyloid deposition was found (DSC

249 Regions showing significant hypometabolism with increasing cortex-wide amyloid burde

250 Accordingly, glucose hypometabolism within the brain may result in disruption