ライフサイエンスコーパス: amyloid deposition

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

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

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

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

5 lin signaling may affect brain metabolism or amyloid deposition.

6 1/3 of healthy elderly have significant beta-amyloid deposition.

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

8 e hitherto mysterious timing and location of amyloid deposition.

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

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

11 s had evidence for neurodegeneration without amyloid deposition.

12 ight spread within the anatomical pattern of amyloid deposition.

13 lusively within areas already affected by BL amyloid deposition.

14 tomography imaging of cerebrocortical abeta-amyloid deposition.

15 peutic strategies aimed at reducing vascular amyloid deposition.

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

17 fibrillogenesis in determining the extent of amyloid deposition.

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

19 ymptoms are coupled to neurodegeneration not amyloid deposition.

20 heimer's disease because it is essential for amyloid deposition.

21 cognitive deterioration and reduced cerebral amyloid deposition.

22 f apoE-containing lipoproteins and decreased amyloid deposition.

23 sociated with regions of dense microvascular amyloid deposition.

24 hanges in the years preceding measurement of amyloid deposition.

25 rotein aggregation with fibril formation and amyloid deposition.

26 nly midlife dyslipidemia was associated with amyloid deposition.

27 ession is an effective strategy to attenuate amyloid deposition.

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

29 n to investigate the spatial distribution of amyloid deposition.

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

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

32 stimulation of neural activity can increase amyloid deposition.

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

34 suggestive of axonal white matter injury and amyloid deposition.

35 ts cortical distribution overlapping that of amyloid deposition.

36 transthyretin mutations causing accelerated amyloid deposition.

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

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

39 ronal activity in vivo significantly reduces amyloid deposition.

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

41 tion between APOE and hippocampal volume and amyloid deposition.

42 2 kinetics specifically in participants with amyloid deposition.

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

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

45 3 or more days per week, was associated with amyloid deposition (31.2% vs 14.7%; P = .03).

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

47 Abeta42 and Abeta40 have opposing effects on amyloid deposition: Abeta42 promotes amyloid deposition

48 80.4% vs 83.7%), compared with those without amyloid deposition, after correction for age, sex, and A

49 factor in predicting progression relative to amyloid deposition alone.

50 s in this study confirmed extensive striatal amyloid deposition, along with typical cortical depositi

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

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

53 1 treatment markedly decreased extracellular amyloid deposition and Abeta1-42/Abeta1-40 ratio, preven

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

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

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

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

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

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

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

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

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

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

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

65 heimer's disease (AD), but their role in the amyloid deposition and cognitive impairment associated w

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

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

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

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

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

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

72 differences in topographical distribution of amyloid deposition and grey matter loss were shown.

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

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

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

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

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

78 e obliteration of the normal architecture by amyloid deposition and little or no vascular or intersti

79 airment by decades, the relationship between amyloid deposition and longitudinal change in neuronal f

80 amyloid deposition in young mice and affect amyloid deposition and memory function in old mice with

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

82 e greatly attenuating the increased vascular amyloid deposition and microhemorrhage observed with unm

83 Amyloid deposition and MRI volumetrics were analyzed in

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

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

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

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

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

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

90 to characterize the effect of metal ions on amyloid deposition and plaque growth on a solid surface,

91 Amyloid deposition and reduced beta-cell mass are pathol

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

93 injury, and there is evidence for increased amyloid deposition and risk for Alzheimer's disease foll

94 Amyloid deposition and tau protein-related neuronal inju

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

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

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

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

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

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

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

102 oxidase in the cerebrovascular alterations, amyloid deposition, and behavioral deficits observed in

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

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

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

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

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

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

109 d imaging to demonstrate that high levels of amyloid deposition are associated with aberrant default

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

111 Brain amyloid depositions are the main hallmarks of Alzheimer'

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

113 It is possible that increased beta-amyloid deposition arises from alterations in amyloid pr

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

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

116 ncreased Abeta42/Abeta40 ratios and enhanced amyloid deposition as previously reported.

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

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

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

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

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

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

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

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

125 ects on amyloid deposition: Abeta42 promotes amyloid deposition but Abeta40 inhibits it.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

146 Amyloid deposition diminished day/night amplitude and li

147 a key step to understanding the mechanism of amyloid deposition diseases including Parkinson's diseas

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

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

150 [11C]PiB PET could be valuable in imaging amyloid deposition following TBI.

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 es regarding how anti-Abeta antibodies alter amyloid deposition have been postulated, yet there is no

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

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

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

160 [11C]PiB PET was used to image amyloid deposition in 11 controls (median [range] age, 3

161 E1 inhibition of Abeta production does lower amyloid deposition in 12-month-old Tg2576 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 kidney is one of the most frequent sites of amyloid deposition in AL, AA, and several of the heredit

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

166 e amyloid-beta peptide and inhibits cerebral amyloid deposition in amyloid-beta precursor protein (AP

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

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

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

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

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

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

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

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

175 -12/23p40 were significantly associated with amyloid deposition in HC, suggesting that these two biom

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

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

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

179 o explore the natural history of preclinical amyloid deposition in people at high risk for AD.

180 sed lipid associated with apoE and increased amyloid deposition in several AD mouse models.

181 sease transmission but elicited striking PrP-amyloid deposition in several recipient mouse brains.

182 ween these options, we reversibly suppressed amyloid deposition in Tg2576 mice with the anti-Abeta an

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

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

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

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

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

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

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

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

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

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

193 Amyloid deposition in the kidney causes progressive dete

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

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

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

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

198 Amyloid deposition in the preclinical stage of AD appear

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

200 ility of accumulated amyloid and exacerbated amyloid deposition in the vasculature.

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

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

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

204 ts, suggesting a role for HSPGs in mediating amyloid deposition in type 2 diabetes and implicating a

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

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

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

208 has been given safely to humans can prevent amyloid deposition in young mice and affect amyloid depo

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

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

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

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

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

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

215 Amyloid deposition is associated with lower cognitive pe

216 Amyloid deposition is associated with premature loss of

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

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

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

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

221 Amyloid deposition is present in 20-50% of nondemented o

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

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

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

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

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

227 Although cerebral amyloid deposition may precede cognitive impairment by d

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

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

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

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

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

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

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

235 The early, focal striatal amyloid deposition observed in these PS1 mutation carrie

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

252 ically distinct between subtypes, but not to amyloid deposition patterns that are diffuse and similar

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

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

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

256 In humans, amyloid deposition precedes the appearance of intracellu

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

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

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

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

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

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

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 ective properties of Abeta40 with respect to amyloid deposition suggest that strategies that preferen

266 Amyloid deposition, tangle formation, neuroinflammation

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

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

269 l imaging to monitor CAA in a mouse model of amyloid deposition to evaluate the effects of anti-Abeta

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

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

272 e absence of dementia, we compared levels of amyloid deposition (via 'Pittsburgh Compound-B' (PIB) po

273 any neurological disease on passage, but PrP-amyloid deposition was again observed in the brains of r

274 Amyloid deposition was assessed using carbon-11-labeled

275 Increased amyloid deposition was associated with beta-cell apoptos

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

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

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

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

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

281 Amyloid deposition was inhibited in vivo by the antibiot

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

283 Amyloid deposition was more extended than hypometabolism

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

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

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

287 vivo effects of RTN3 and preformed RIDNs on amyloid deposition, we crossed bitransgenic mice express

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

289 (11)C-PIB images of amyloid deposition were acquired on average 10.8+/-0.8 y

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

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

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

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

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

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

298 ors including IL-1 beta co-localized to beta-amyloid depositions within myofibres.

299 We hypothesized that amyloid deposition would be observed with PiB in CAA, an

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