ライフサイエンスコーパス: amyloid deposition

1 in a transgenic mouse model (5xFAD) of early amyloid deposition.

2 pse loss, and microglial activation, but not amyloid deposition.

3 suggestive of axonal white matter injury and amyloid deposition.

4 transthyretin mutations causing accelerated amyloid deposition.

5 ging in relation to age, cognition, and beta-amyloid deposition.

6 age, long before memory impairments or beta-amyloid deposition.

7 ronal activity in vivo significantly reduces amyloid deposition.

8 ed neurovascular dysfunction and in vascular amyloid deposition.

9 served in this population is not due to beta-amyloid deposition.

10 tion between APOE and hippocampal volume and amyloid deposition.

11 2 kinetics specifically in participants with amyloid deposition.

12 o the ages of participants and the amount of amyloid deposition.

13 as observed from the earliest stages of beta-amyloid deposition.

14 mple spike activity prior to cerebellar beta-amyloid deposition.

15 tosis and iron deposition around plaque-like amyloid deposition.

16 ons, and a characteristic pattern of hepatic amyloid deposition.

17 lin signaling may affect brain metabolism or amyloid deposition.

18 dividual ABX or an ABX cocktail and assessed amyloid deposition.

19 1/3 of healthy elderly have significant beta-amyloid deposition.

20 tum and thalamus to be the earliest sites of amyloid deposition.

21 e hitherto mysterious timing and location of amyloid deposition.

22 MP-2 and MMP-9 play a role in reducing islet amyloid deposition.

23 rstitial fluid Abeta, but not the effects on amyloid deposition.

24 s had evidence for neurodegeneration without amyloid deposition.

25 ight spread within the anatomical pattern of amyloid deposition.

26 lusively within areas already affected by BL amyloid deposition.

27 tomography imaging of cerebrocortical abeta-amyloid deposition.

28 peutic strategies aimed at reducing vascular amyloid deposition.

29 en in-vivo and histological measures of beta-amyloid deposition.

30 fibrillogenesis in determining the extent of amyloid deposition.

31 against the AD phenotype in a mouse model of amyloid deposition.

32 ymptoms are coupled to neurodegeneration not amyloid deposition.

33 al synaptic transmission in a mouse model of amyloid deposition.

34 rodegenerative diseases are characterized by amyloid deposition.

35 bution in PRS risk predictions of AD/MCI and amyloid deposition.

36 degenerative pathologies resulting from beta-amyloid deposition.

37 term synaptic plasticity and memory, or from amyloid deposition.

38 ed tau concentrations specifically predicted amyloid deposition.

39 ntly for distinguishing between AD, MCI, and amyloid deposition.

40 eta (oAbeta) but no histological evidence of amyloid deposition.

41 ts cortical distribution overlapping that of amyloid deposition.

42 ingly, this effect was observed before overt amyloid deposition.

43 nly midlife dyslipidemia was associated with amyloid deposition.

44 n to investigate the spatial distribution of amyloid deposition.

45 t on neurodegeneration in AD regions than on amyloid deposition.

46 tion of apoE levels after birth would affect amyloid deposition.

47 stimulation of neural activity can increase amyloid deposition.

48 3 or more days per week, was associated with amyloid deposition (31.2% vs 14.7%; P = .03).

49 sease are all caused by mutations which make amyloid deposition a more likely event.

50 grouping the markers into three categories: amyloid deposition (A), tauopathy (T), and neurodegenera

51 80.4% vs 83.7%), compared with those without amyloid deposition, after correction for age, sex, and A

52 factor in predicting progression relative to amyloid deposition alone.

53 ]) but not in patients with high parenchymal amyloid deposition (Alzheimer disease [AD]; mild cogniti

54 After controlling for amyloid deposition, amplitude of Abeta40 was positively

55 1 treatment markedly decreased extracellular amyloid deposition and Abeta1-42/Abeta1-40 ratio, preven

56 ncy in mice expressing human APP accelerates amyloid deposition and behaviour deficits.

57 ereas when neprilysin was up-regulated islet amyloid deposition and beta-cell apoptosis both decrease

58 Following neprilysin inhibition, islet amyloid deposition and beta-cell apoptosis increased by

59 ion of MMP-9 in amyloid-prone islets reduced amyloid deposition and beta-cell apoptosis.

60 tes, thereby contributing to increased islet amyloid deposition and beta-cell loss.

61 The relationship between amyloid deposition and cellular toxicity is still contro

62 al volume in MRI markers, increased cerebral amyloid deposition and cerebral hypometabolism.

63 zheimer's disease: hippocampal volume, brain amyloid deposition and cerebral metabolism.

64 the effect of chronic high fat diet (HFD) on amyloid deposition and cognition of 12-months old APP23

65 mice and examined Abca1 gene dose effect on amyloid deposition and cognition.

66 peptides in human brains leads to increased amyloid deposition and cognitive dysfunction, which are

67 ack of strong association between brain beta-amyloid deposition and cognitive impairment has been a c

68 Furthermore, abdominal fat aspiration showed amyloid deposition and confirmed the diagnosis of amyloi

69 In Alzheimer's disease patients, although amyloid deposition and CSF amyloid changes continued to

70 omarkers predicted each other, although both amyloid deposition and CSF tau progression predicted cog

71 an age when the AD transgenics display early amyloid deposition and few cholinergic defects, and 10-m

72 uroinflammation is associated with localized amyloid deposition and glucose metabolism over time, how

73 associations with cognitive measures, brain amyloid deposition and glucose metabolism.

74 tomography scans for microglial activation, amyloid deposition and glucose metabolism.

75 to examine longitudinal regional patterns of amyloid deposition and hypometabolism in the same popula

76 increased risk of Alzheimer's disease (AD), amyloid deposition and hypometabolism.

77 mer's disease was positively correlated with amyloid deposition and inversely correlated with regiona

78 islet MMP-9 activity could reduce or prevent amyloid deposition and its toxic effects in type 2 diabe

79 endogenous islet protease that limits islet amyloid deposition and its toxic effects via degradation

80 ent of RU-505 significantly reduced vascular amyloid deposition and microgliosis in the cortex and im

81 Amyloid deposition and MRI volumetrics were analyzed in

82 eeding stage of amyloid development enhanced amyloid deposition and neuritic dystrophy in amyloid mod

83 polygenic hazard scores were associated with amyloid deposition and neurodegeneration in susceptible

84 D, we evaluated the association between beta-amyloid deposition and neuroinflammation in AD.

85 A clear positive correlation between beta-amyloid deposition and neuroinflammation was detected wi

86 To monitor the longitudinal changes in beta-amyloid deposition and neuroinflammation, we used in viv

87 iminary results indicate that CSF markers of amyloid deposition and neuronal injury in early Alzheime

88 Amyloid deposition and neuronal loss were significantly

89 atment, thus preventing or retarding further amyloid deposition and organ damage.

90 Amyloid deposition and reduced beta-cell mass are pathol

91 For example, amyloid deposition and reduced metabolism is seen early

92 Amyloid deposition and tau protein-related neuronal inju

93 is likely to be beneficial by reducing both amyloid deposition and the formation RIDNs.

94 atures: (i) dissociation between the rate of amyloid deposition and the rate of neurodegeneration lat

95 Our data suggest that CD36 promotes vascular amyloid deposition and the resulting cerebrovascular dam

96 wed that the enzyme neprilysin reduces islet amyloid deposition and thereby reduces beta-cell apoptos

97 ort BACE1 inhibition as concretely impacting amyloid deposition and therefore potentially an importan

98 in TgCRND8 markedly decreased extracellular amyloid deposition and total brain amyloid-beta peptide

99 y elderly subjects and manifests by signs of amyloid deposition and/or neuronal injury in the brain,

100 iomarkers, amyloid-PET, which assesses brain amyloid deposition, and (18)F-fluorodeoxyglucose ((18)F-

101 emical markers of Alzheimer's disease, brain amyloid deposition, and brain metabolism as well as prog

102 ate the association between tau aggregation, amyloid deposition, and cognitive function.

103 relationship between microglial activation, amyloid deposition, and glucose metabolism in Parkinson'

104 hyperphosphorylated tau, neuroinflammation, amyloid deposition, and neuronal death in vitro and in v

105 d role of CD36 in the mechanisms of vascular amyloid deposition, and suggest that this scavenger rece

106 e models in a transgenic mouse model of beta-amyloid deposition (APPswe/PS1dE9).

107 Endogenous priming and bulk amyloid deposition are thus separable events, each sensi

108 Brain amyloid depositions are the main hallmarks of Alzheimer'

109 tosis and microgliosis diverges from that of amyloid deposition, arguing against a straightforward re

110 ity, rescues neurovascular coupling, reduces amyloid deposition around blood vessels, and improves co

111 We evaluated the role of cortical amyloid deposition as a factor contributing to memory dy

112 iagnostic accuracy of glucose metabolism and amyloid deposition as demonstrated by (18)F-FDG and Pitt

113 The presence of extracellular beta-amyloid deposition as neuritic plaques and intracellular

114 of dementia, characterised by extracellular amyloid deposition as plaques and intracellular neurofib

115 (AD) has been widely demonstrated to resolve amyloid deposition as well as associated neuronal, glial

116 Amyloid deposition, as assessed by Abeta42 levels, was p

117 between levels of microglial activation and amyloid deposition at a voxel level were assessed using

118 SUVrs and 3 different pathologic measures of amyloid deposition at autopsy using all 4 reference regi

119 th (18)F-FDG, was seen and may suggest early amyloid deposition before cerebral metabolic disruption

120 in young adults and examined differences in amyloid deposition between these regions across groups.

121 c antibodies has been demonstrated to reduce amyloid deposition both in vitro and in vivo Because N-t

122 presenilins (PS) 1 and 2 are associated with amyloid deposition, brain structural change and cognitiv

123 T(D) inhibits Abeta aggregation and cerebral amyloid deposition, but a long treatment schedule unexpe

124 HJ6.3 dramatically decreased amyloid deposition by 60-80% and significantly reduced i

125 adults aged 60 to 87 years with and without amyloid deposition by a novel precise mass spectrometry

126 tions (FAD-Tg), 5xFAD-Tg mice, which exhibit amyloid deposition by age 2 months, were crossed with ap

127 To determine if neprilysin modulated amyloid deposition by cleaving hIAPP, analysis of hIAPP

128 In summary, neprilysin decreases islet amyloid deposition by inhibiting hIAPP fibril formation,

129 Biomarkers of brain Abeta amyloid deposition can be measured either by cerebrospin

130 c expression of SAA in mice, we show that AA amyloid deposition can occur independently of inflammati

131 tosolic protein folding by assessing whether amyloid deposition causes normally soluble proteins to m

132 According to this theory, amyloid deposition causes severe damage to neurons many

133 eukoaraiosis) in patients with high vascular amyloid deposition (cerebral amyloid angiopathy [CAA]) b

134 Advanced cerebrovascular beta-amyloid deposition (cerebral amyloid angiopathy, CAA) is

135 terin, vitronectin, and fibromodulin) and of amyloid deposition (clusterin, alpha2-macroglobulin, and

136 ound that 5XFAD/Tg197 mice display decreased amyloid deposition, compromised neuronal integrity, and

137 ised amyloidosis classified as biopsy proven amyloid deposition confined to one site or tissue proven

138 d beta-cell apoptosis, suggesting that islet amyloid deposition contributes to the decreased beta-cel

139 althy elderly, CSF amyloid changes predicted amyloid deposition, CSF phosphorylated tau concentration

140 d into this sequence, but reconfigured as an amyloid deposition cycle.

141 Diabetes was associated with increased amyloid deposition, decreased beta-cell area, and increa

142 ly normal individuals at different stages of amyloid deposition defined by longitudinal amyloid imagi

143 thin single amyloid plaques correlating with amyloid deposition density and the measurement of hippoc

144 Amyloid deposition diminished day/night amplitude and li

145 Many current models of amyloid deposition diseases posit that the most toxic sp

146 mer's neuropathology and (3) fibrillar brain amyloid deposition during aging.

147 n important role for DHA metabolism in brain amyloid deposition during the preclinical or early sympt

148 ex has the strongest association with AD and amyloid deposition even when genes in the APOE region we

149 [11C]PiB PET could be valuable in imaging amyloid deposition following TBI.

150 eplenish neuronal loss but also for reducing amyloid deposition for Alzheimer's treatment.

151 ors were not associated with late-life brain amyloid deposition (for >/=2 late-life vascular risk fac

152 We aimed to assess the relationship between amyloid deposition, glucose metabolism and ApoE4 genotyp

153 This study assessed the relationship between amyloid deposition, glucose metabolism and clinical phen

154 on overall in this group, this suggests that amyloid deposition has an early and subclinical impact o

155 Thus we conclude that regional fibrillar amyloid deposition has little to no association with reg

156 rates the cardinal features of AD, including amyloid deposition, hyperphosphorylated and aggregated t

157 ed (1) cross-sectional relationships between amyloid deposition, hypometabolism, and cognition, and (

158 ng biomarkers of Alzheimer's disease include amyloid deposition [imaged with [(11)C]Pittsburgh compou

159 [11C]PiB PET was used to image amyloid deposition in 11 controls (median [range] age, 3

160 E1 inhibition of Abeta production does lower amyloid deposition in 12-month-old Tg2576 mice.

161 ction; and ameliorated neuroinflammation and amyloid deposition in AD mice.

162 ssion is a potential approach for inhibiting amyloid deposition in AD patients.

163 duces hepatic APOC3 transcription, may delay amyloid deposition in affected patients.

164 nk between HTRA1, complement regulation, and amyloid deposition in AMD pathogenesis.

165 of the protease neprilysin completely arrest amyloid deposition in an aggressively depositing transge

166 The distribution and extent of amyloid deposition in body organs establishes the progno

167 d in a gene dose-dependent reduction in beta-amyloid deposition in both the APPPS1 and R1.40 mouse mo

168 Quantification of ECV measures cardiac amyloid deposition in both types of amyloidosis and show

169 ebral amyloid angiopathy, the result of beta-amyloid deposition in cerebral vessels.

170 ta40 or Abeta42:tau ratios as a biomarker of amyloid deposition in clinical practice and trials.

171 We found that amyloid deposition in cortex, the hippocampal CA3 region

172 -B ((11)C-PIB) PET images to detect cortical amyloid deposition in different memory clinic patient gr

173 -12/23p40 were significantly associated with amyloid deposition in HC, suggesting that these two biom

174 ic variant within RNF219 was found to affect amyloid deposition in human brain and LOAD age-of-onset.

175 fractalkine signaling leads to reduced beta-amyloid deposition in mouse models of AD that is potenti

176 the association between rs3818361 and brain amyloid deposition in nondemented older individuals.

177 florbetapir PET/CT detected widespread organ amyloid deposition in subjects with both active AL and A

178 us (AAV) vector, decreased parenchymal Abeta amyloid deposition in TgCRND8 mice and ADan (Danish Amyl

179 he findings suggest that HSPGs contribute to amyloid deposition in tgSwe mice by increasing Abeta fib

180 ute exposure to HJ6.3 affected the course of amyloid deposition in that it prevented the formation of

181 be implicated in the mechanism that leads to amyloid deposition in the atherosclerotic plaques in viv

182 ogic dysfunction characterized by widespread amyloid deposition in the brain and the presence of a sh

183 ed that ARB use is associated with decreased amyloid deposition in the brain in Alzheimer's disease a

184 transgenic mice, Abca1 deficiency increased amyloid deposition in the brain paralleled by decreased

185 c transmission of amyloid beta might lead to amyloid deposition in the brain parenchyma and blood ves

186 itro studies also indicate that DHA prevents amyloid deposition in the brain.

187 The feasibility of detecting tau and amyloid deposition in the brains of living persons at ri

188 The progression of beta-amyloid deposition in the brains of mice overexpressing

189 However, reduction of amyloid deposition in the hippocampal CA1 region, where

190 For example, amyloid deposition in the neocortex precedes the spread

191 is a strikingly greater variability in brain amyloid deposition in the noncarrier group relative to r

192 The basis and role of amyloid deposition in the pathogenesis of these diseases

193 by neocortical [3H]PiB binding in regions of amyloid deposition in the postmortem tissue of patients

194 Amyloid deposition in the preclinical stage of AD appear

195 y studies have suggested early and prominent amyloid deposition in the striatum in presenilin 1 mutat

196 ibrillary tangles coexist with extensive pre-amyloid deposition in the virtual absence of fibrillar l

197 roduction of human APOE significantly delays amyloid deposition in transgenic mice expressing familia

198 eloid cells with peripheral monocytes alters amyloid deposition in two mouse models of cerebral beta-

199 ovel approach to reduce and/or prevent islet amyloid deposition in type 2 diabetes.

200 f the very limited possibility of diagnosing amyloid deposition in vivo, which until recently require

201 apolipoprotein C-III does not contribute to amyloid deposition in vivo.

202 isease accompanied with widespread brain PrP amyloid deposition, in the absence of spongiform changes

203 In the atherosclerotic plaques, amyloid deposition increases with aging.

204 occurred in the absence of changes in islet amyloid deposition, indicating ARC acts downstream of am

205 odels has made it difficult to establish how amyloid deposition initiates the cascade of events that

206 we also observed similar rs73069071-by-beta-amyloid deposition interaction effect on global cognitiv

207 e 2 diabetes; however, whether the extent of amyloid deposition is associated with decreased beta-cel

208 Amyloid deposition is associated with lower cognitive pe

209 Amyloid deposition is associated with premature loss of

210 This correlation suggests that neocortical amyloid deposition is connected to or even drives neuron

211 tly of inflammation and that the time before amyloid deposition is determined by the circulating SAA

212 se risk factors directly contribute to brain amyloid deposition is less well understood.

213 in both types of amyloidosis and shows that amyloid deposition is more extensive in patients with AT

214 Amyloid deposition is predicted by APOE only (AUC = 79%)

215 The hypothesis that amyloid deposition is the leading cause of Alzheimer's d

216 Brain amyloid deposition is thought to be a seminal event in A

217 were primed, especially for rapid glomerular amyloid deposition leading to renal failure, closely res

218 Cardiac amyloid deposition leads to an infiltrative or restricti

219 ngly, ASO treatment starting at the onset of amyloid deposition led to an increase in Abeta plaque si

220 hanisms active in sleep-wake cycles and that amyloid deposition may impair normal circadian patterns.

221 Small vessel disease (SVD) and amyloid deposition may promote each other, with a potent

222 ion of AD and, in the context of significant amyloid deposition, may provide a second hit necessary f

223 positron emission tomography [FDG-PET]) and amyloid deposition (measured by [(11)C] Pittsburgh Compo

224 tions between plasma Abeta42 and neocortical amyloid deposition (measured with PET).

225 factors are associated with late-life brain amyloid deposition, measured using florbetapir positron

226 SNPs in the APOE gene (i.e. top AD gene) and amyloid deposition measures among cortical regions (i.e.

227 nstrate that strokes can trigger accelerated amyloid deposition, most likely through interference wit

228 age-at-disease-onset, clinical progression, amyloid deposition, neurofibrillary tangles, and composi

229 synthesis, whereas in systemic amyloidosis, amyloid deposition occurs distant from the site of precu

230 Systemic amyloid deposition of aggregated transthyretin causes he

231 scade and the aging-associated extracellular amyloid deposition of FAF.

232 of normal controls, both the main effect of amyloid deposition of worse memory performance and the i

233 Amyloid deposition of WT human beta(2)-microglobulin (WT

234 e Alzheimer's disease and showed evidence of amyloid deposition on (11)C-labelled Pittsburgh compound

235 All PCA subjects showed beta-amyloid deposition on PET scanning.

236 compared to AD, and its relationship to beta-amyloid deposition on PET.

237 and 12% of ADNI-1 subjects had evidence for amyloid deposition only, whereas 43% of MCSA and 55% of

238 ific MMP-2 inhibitor had no effect on either amyloid deposition or beta-cell apoptosis.

239 grade beta-amyloid, we observed no increased amyloid deposition or increased incidence of dementia in

240 neration in TgF344-AD rats, without altering amyloid deposition or indicators of neuroinflammation.

241 ignificant differences in global or regional amyloid deposition or neuronal metabolic deficit between

242 Age at onset does not influence amyloid deposition or neuronal metabolic deficit in AD.

243 PET imaging evidence of significant cerebral amyloid deposition or nigrostriatal denervation was a st

244 le amyloid load, and 2 (5%) showed increased amyloid deposition over the followup period.

245 We measured change in amyloid deposition over time using serial (11)C Pittsbur

246 of apoA-I cause protein destabilization and amyloid deposition, oxidative conditions similar to thos

247 d higher education were associated with less amyloid deposition (p = .014).

248 urrent research in the detection of regional amyloid deposition patterns and its potential for stagin

249 CSF) levels of beta-amyloid peptide (A, beta-amyloid deposition), phosphorylated tau (T, pathologic t

250 n participants without preclinical fibrillar amyloid deposition (PIB-).

251 f serum DHA levels together with measures of amyloid deposition (Pittsburgh Compound B index), brain

252 and 55% of ADNI-1 subjects had evidence for amyloid deposition plus neurodegeneration (magnetic reso

253 In humans, amyloid deposition precedes the appearance of intracellu

254 E), the skin changes were found to be due to amyloid deposition primarily around the pilosebaceous un

255 rate of neurodegeneration late in life, with amyloid deposition proceeding at a constant slow rate wh

256 verse correlation between beta-cell area and amyloid deposition (r = -0.42, P < 0.001).

257 We analysed regional patterns of amyloid deposition, regional glucose metabolism and regi

258 cation of patterns of glucose metabolism and amyloid deposition related to the conversion from mild c

259 ripheral inhibition of huTNF-alpha increases amyloid deposition, rescues neuronal impairment, and sup

260 of AD, mild cognitive impairment (MCI), and amyloid deposition risks with PRS, including and excludi

261 me in APOE3 and APP/APOE3 mice revealed that amyloid deposition significantly affects the response to

262 performance did not predict concurrent beta-amyloid deposition, small vessel disease or Alzheimer's

263 rtical clusters of microglial activation and amyloid deposition spatially overlapped in the subjects

264 Indicators of amyloid deposition such as (11)C-Pittsburgh compound B (

265 and progression of diseases associated with amyloid deposition, such as Parkinson's and Alzheimer's

266 between basal forebrain RSFC and the global amyloid deposition (t values >3.59; P <.05 corrected for

267 Amyloid deposition, tangle formation, neuroinflammation

268 we constructed a model combining markers for amyloid deposition, tauopathy, and neurodegeneration (AT

269 eta amyloidosis results in greater Abeta and amyloid deposition than with apoE3 expression.

270 In amyloid precursor protein (APP) models of amyloid deposition, the amount of amyloid deposits incre

271 dels of age-associated memory impairment and amyloid deposition to study transcriptome and cell type-

272 is day/night pattern attenuates with age and amyloid deposition, to our knowledge, the association of

273 Amyloid deposition was assessed using carbon-11-labeled

274 Increased amyloid deposition was associated with beta-cell apoptos

275 This reduced vascular amyloid deposition was associated with preservation of t

276 mice expressing Swedish APP and PS1DeltaE9, amyloid deposition was clearly reduced (0.66% of total m

277 in neocortical gray matter, in regions where amyloid deposition was demonstrated by immunocytochemist

278 as applied to the brain cortical surface and amyloid deposition was followed over 2 weeks using in vi

279 ased similarity of FU hypometabolism with BL amyloid deposition was found (DSC: 47%).

280 Amyloid deposition was inhibited in vivo by the antibiot

281 progressively higher levels of CR, increased amyloid deposition was less or not at all associated wit

282 ers of cognitive aging and AD, cortical beta-amyloid deposition was lower in MS than age-matched cont

283 Amyloid deposition was more extended than hypometabolism

284 Although amyloid deposition was not observed in TGFBI-R124C mice,

285 beta42 levels were used to determine whether amyloid deposition was present or absent.

286 s characterized using graph theory and brain amyloid deposition was quantified by Pittsburgh compound

287 ion, where RIDNs predominantly formed before amyloid deposition, was less significant.

288 h occurs before the detectable reductions in amyloid deposition, we hypothesize that the IVIg and poo

289 This inflammation and beta-amyloid deposition were associated with reactive microgl

290 ing human IAPP dramatically accelerates IAPP amyloid deposition, which was accompanied by clinical ab

291 tion is that APOE-epsilon4 promotes vascular amyloid deposition, while APOE-epsilon2 promotes progres

292 ntly to lipid homeostasis, inflammation, and amyloid deposition, while CD36 deficiency is associated

293 t no evidence that it predicted in vivo beta-amyloid deposition, white matter hyperintensity volume,

294 ly under way to determine whether preventing amyloid deposition will be beneficial in arresting progr

295 ge any effective treatment aimed at reducing amyloid deposition will probably be too late.

296 Intervention into amyloid deposition with anti-amyloid agents like the pol

297 D, seems to follow the anatomical pattern of amyloid deposition with temporal delay.

298 a phase II study (n = 72) were used to model amyloid deposition with the investigational PET imaging

299 typical patterns of BL hypometabolism and BL amyloid deposition, with a similarity of 40% (DSC).

300 ions in the gut microbiome may contribute to amyloid deposition, yet the microbial communities associ