ライフサイエンスコーパス: hypometabolism

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

2 sed cerebral amyloid deposition and cerebral hypometabolism.

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

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

5 and fat mass before LTx was associated with hypometabolism.

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

7 exhibits mild obesity without hyperphagia or hypometabolism.

8 t significantly related to either atrophy or hypometabolism.

9 al activity is reflected by cortical glucose hypometabolism.

10 pection and presented in previous reports of hypometabolism.

11 ecuneus), strongly overlapping with regional hypometabolism.

12 th IDU, resulting in more extensive cortical hypometabolism.

13 ) F]FDG uptake, which showed more widespread hypometabolism.

14 c cytochrome oxidase contributions to energy hypometabolism.

15 ellar hypometabolism and 13% had ipsilateral hypometabolism.

16 lism, whereas 15% had ipsilateral cerebellar hypometabolism.

17 ed isolated bilateral anterior temporal lobe hypometabolism.

18 more restricted distribution than an area of hypometabolism.

19 were associated with ipsilateral cerebellar hypometabolism.

20 were associated with ipsilateral cerebellar hypometabolism.

21 me in the presence of bilateral temporal PET hypometabolism.

22 gly different posterior-occipital pattern of hypometabolism.

23 rgely identical patterns of temporo-parietal hypometabolism.

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

25 rovement of clinical symptoms and cerebellar hypometabolism.

26 ich neuroimaging has linked to brain glucose hypometabolism.

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

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

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

30 ending the larval development period through hypometabolism.

31 n has little to no association with regional hypometabolism.

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

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

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

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

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

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

38 HPRT1 uniquely showed glucose hypometabolism across all nine cerebral regions.

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

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

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

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

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

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

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

46 einopathies and clinicopathologic factors on hypometabolism and atrophy.

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

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

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

50 n (18)F-AV-45 SUV ratio (SUVr) in regions of hypometabolism and elevated amyloid load typical of AD,

51 Greater hypometabolism and flortaucipir uptake were also observe

52 Brain aging is associated with hypometabolism and global changes in functional connecti

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

54 were performed for regions with significant hypometabolism and hypermetabolism.

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

56 intenance of core temperature), resulting in hypometabolism and hypothermia.

57 Cerebral hypometabolism and impaired episodic memory were observe

58 ortex confirmed overall associations between hypometabolism and local tau pathology and thickness and

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

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

61 ical aging are associated with brain glucose hypometabolism and mitochondrial adaptations in female b

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

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

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

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

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

67 imaging abnormalities, with greater atrophy, hypometabolism and white matter tract degeneration in th

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

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

70 ging (MRI) findings, concordant (18) FDG-PET hypometabolism, and at least 2 years of postoperative fo

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

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

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

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

75 ted with regional EEG abnormalities, FDG-PET hypometabolism, and elevated velocities on transcranial

76 89 years) who were negative for amyloidosis, hypometabolism, and hippocampal atrophy.

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

78 positron emission tomography ((18) FDG-PET) hypometabolism, and seizure outcomes in patients with un

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

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

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

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

83 term cases had cerebellar and insula glucose hypometabolism as well as parietal glucose hypermetaboli

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

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

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

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

88 Brain (18)F-FDG PET showed diffuse cortical hypometabolism associated with putaminal and cerebellum

89 k destabilization may reflect early signs of hypometabolism, associated with dementia.

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

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

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

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

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

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

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

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

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

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

100 -tau205 and t-tau) increase with atrophy and hypometabolism closer to symptom onset.

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

102 In FDG-PET, AD+LB+ showed more severe hypometabolism compared to AD+LB-, but both groups were

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

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

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

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

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

108 Hypometabolism extended over wider regions than hypoperf

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

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

111 mutation in OATP1C1 is associated with brain hypometabolism, gradual neurodegeneration, and impaired

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

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

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

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

116 sy (PSP) include midbrain atrophy in MRI and hypometabolism in [(18)F]fluorodeoxyglucose (FDG)-positr

117 [18F]fluorodeoxyglucose revealed widespread hypometabolism in a pattern found in sporadic multiple s

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

135 ain's default mode network leads to regional hypometabolism in distant but functionally connected bra

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

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

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

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

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

141 ate doses can induce profound but reversible hypometabolism in mammals.

142 ns in the MPA can coordinate hypothermia and hypometabolism in mice.

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

144 showed perirolandic and variable prefrontal hypometabolism in most patients.

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

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

147 ons between medial temporal degeneration and hypometabolism in retrosplenial, orbitofrontal and anter

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

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

150 features were associated with more prominent hypometabolism in specific regions, thus suggesting a cl

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

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

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

154 zes the reactive astrocyte-mediated neuronal hypometabolism in the brains with neuroinflammation and

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

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

157 to the control cohort revealed a significant hypometabolism in the left temporal lobe (BAs 20, 36 and

158 ith the control cohort, revealed significant hypometabolism in the left temporal lobe (Brodmann areas

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

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

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

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

163 As hypometabolism in the patients' rostral fusiform was eve

164 Hypometabolism in the posterior parietal cortex (PPC) is

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

166 trols, HIVMSM and PrEPMSM exhibited a common hypometabolism in the prefrontal cortex that correlated

167 Extensive hypometabolism in the prefrontal or anterior temporal ar

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

169 There was hypometabolism in the right superior temporal gyrus and

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

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

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

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

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

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

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

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

178 Cerebral areas showing hypometabolism include those known to be affected in dem

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

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

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

182 Patients with thalamic hypometabolism ipsilateral to the removed temporal lobe

183 Regional glucose hypometabolism is a defining feature of Alzheimer diseas

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

185 Occipital hypometabolism is a potential antemortem marker to disti

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

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

188 Striatal hypometabolism is associated with clinical disease sever

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

190 Brain hypometabolism is associated with the clinical consequen

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

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

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

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

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

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

197 ing animals living in seasonal environments, hypometabolism (lowered metabolic rate) and hypothermia

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

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

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

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

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

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

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

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

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

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

208 Cerebral hypometabolism, mitochondrial dysfunction, and beta-amyl

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

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

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

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

213 Focal glucose hypometabolism of the pallidi, putamina or both, was the

214 19 (COVID-19) and can be related to cortical hypometabolism on (18)F-FDG PET at the subacute stage.

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

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

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

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

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

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

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

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

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

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

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

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

227 orodeoxyglucose positron emission tomography hypometabolism, or both).

228 Regional hypometabolism overlaps to a large degree between PCA an

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

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

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

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

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

234 e profile and a distinct posterior-occipital hypometabolism pattern characteristic for LB disease.

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

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

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

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

239 Hypometabolism progressed over time in almost all subjec

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

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

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

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

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

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

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

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

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

249 Atrophy and hypometabolism significantly correlated in the hippocamp

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

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

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

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

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

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

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

257 Groups susceptible to T had more hypometabolism than expected given T and exhibited worse

258 Groups resilient to T had less hypometabolism than expected relative to T and displayed

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

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

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

262 TL volume and the volume of resected TL PET hypometabolism (TLH) were calculated from the pre- and p

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

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

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

266 Early ictal hypometabolism, transient decreases in cell swelling and

267 ed pattern of pronounced posterior-occipital hypometabolism typical for dementia with LB (DLB), and b

268 ing with metabolic lesions-discrete areas of hypometabolism typically seen on interictal 18F-fluorode

269 Regional hypometabolism was assessed compared with a control coho

270 Prefrontal hypometabolism was associated with reduced clinical func

271 is of 26 individuals, bifrontal cortical FDG hypometabolism was associated with worse Clinical Dement

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

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

274 Frontal lobe hypometabolism was found in SGCE, HPRT1 and PANK2.

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

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

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

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

279 Hypometabolism was most commonly observed in the parieta

280 Conclusion: Frontal hypometabolism was observed in a dysexecutive presentati

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

282 Hypometabolism was observed in heteromodal cortices in d

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

284 Extensive frontotemporal hypometabolism was predictive for a lower survival using

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

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

287 In right MTLE patients, CTL hypometabolism was the strongest predictor of an unfavor

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

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

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

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

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

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

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

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

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

297 nd 5xFAD mouse brains showed signs of fucose hypometabolism with impaired l-fucose signaling.

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

299 r, we found that an interaction between this hypometabolism with overlapping Abeta aggregation is ass

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