ライフサイエンスコーパス: DLB

1 polymorphisms in an additional cohort of 108 DLB cases and 75545 controls from Iceland.

2 e, 72 y; interquartile range, 6.25 y) and 11 DLB patients (median age, 76 y; interquartile range, 10.

3 fied as having Alzheimer's disease (n = 11), DLB (n = 23) or VCI (n = 12).

4 ine transporter (DAT) binding in FTD (n=12), DLB (n=10) and AD (n=9) by visually rating the caudate a

5 All PD and all but 2 DLB samples were also positive for alphaSyn aggregates b

6 ls" or NLs), 114 MCI, 199 AD, 98 FTD, and 27 DLB patients, collected at 7 participating centers.

7 Four DLB patients with apathy and 4 DLB patients without apathy were identified.

8 gnoses of probable (n=94) or possible (n=57) DLB or non-DLB dementia (n=147) established by a consens

9 enty-four patients with Lewy body disease (7 DLB, 8 PD-impaired, and 9 PD-normal) underwent multimoda

10 udy in Norwegian and European cohorts of 720 DLB cases and 6490 controls and included 19 top-associat

11 The cohort comprised 788 DLB cases and 2624 controls.

12 Overall the study included 828 DLB cases and 82035 controls.

13 eloped that correctly classified 95% AD, 92% DLB, 94% FTD, and 94% NL.

14 gnosis of pure DLB (n=12), mixed DLB and AD (DLB+AD n=23) and pure AD (n=89) who had Clinical Dementi

15 t reliably and selectively distinguishes AD, DLB, FTD, and HC, representing a useful additional scree

16 g the most common EPMS in both FTD (83%) and DLB (70%).

17 accuracy of differentiating AD (n = 97) and DLB (n = 47) increased from approximately 85% to approxi

18 Delirium and DLB share a number of clinical similarities, including g

19 Delirium and DLB share a number of features and we hypothesise that d

20 ion and pathophysiology between delirium and DLB, and explore possible links between these diagnoses.

21 em brains of normal, Alzheimer's disease and DLB patients.

22 ranged from absent hypometabolism to FTD and DLB PET patterns.

23 association between rare variants in GRN and DLB.

24 as lipid-associated proteins from normal and DLB brain lysates, and from normal human cerebrospinal f

25 PCA and DLB showed overlapping patterns of hypometabolism involv

26 Results: PCA and DLB showed overlapping patterns of hypometabolism involv

27 m overlaps to a large degree between PCA and DLB, although the degree of involvement of the frontal a

28 m overlaps to a large degree between PCA and DLB, although the degree of involvement of the frontal a

29 ngulate island sign differed between PCA and DLB.

30 In the human PD and DLB brain, calpain-cleaved alpha-Syn antibodies immunola

31 with cortical Lewy bodies in sporadic PD and DLB brains.

32 h activated calpain in neurons of the PD and DLB brains.

33 ent falls and postural instability in PD and DLB but not in MSA.

34 m CON, and was significantly lower in PD and DLB compared to MSA.

35 ostmortem tissues of individuals with PD and DLB compared with healthy controls.

36 n human postmortem brain samples from PD and DLB patients as well as in the brains of alpha-synuclein

37 ociation with cognitive impairment in PD and DLB, conflicting association in PAF, and no association

38 In the clinical continuum between PD and DLB, patients with GBA mutations seem to localize midway

39 lpain-cleavage of alpha-Syn occurs in PD and DLB, we designed site-directed calpain-cleavage antibodi

40 o cognitive impairment or dementia in PD and DLB.

41 rease in DNA methylation reported for PD and DLB.

42 s genetically linked to rare cases of PD and DLB.

43 Furthermore, PDD and DLB may in fact represent 1 overlapping disease entity,

44 ational cohort of patients with PD, PDD, and DLB and healthy controls.

45 Our data show that PD, PDD, and DLB, rather than a disease continuum, have distinct gene

46 ion between GBA1 mutation carrier status and DLB, with an odds ratio of 8.28 (95% CI, 4.78-14.88).

47 , namely 273 patients diagnosed as AD, 67 as DLB, and 207 as FTD, and 147 healthy controls (HC).

48 tion and has revealed an association between DLB and genes such as GBA.

49 rtant pathophysiological differences between DLB and those with mixed Alzheimer's disease/DLB and Alz

50 t test measures did not discriminate between DLB+AD and pure AD.

51 definition of DLB; the relationship between DLB and other neurodegenerative conditions; current unde

52 e hypothesised that, using blood biomarkers, DLB would show an increased proinflammatory profile comp

53 out dementia, AD, dementia with Lewy bodies (DLB) and healthy controls.

54 individuals with dementia with Lewy bodies (DLB) and in more than 50% of AD cases.

55 that include PD, dementia with Lewy bodies (DLB) and multiple system atrophy (MSA).

56 n's disease (PD), dementia with Lewy bodies (DLB) and multiple system atrophy (MSA).

57 kinson's disease, dementia with Lewy bodies (DLB) and multiple system atrophy are characterized by th

58 ive impairment in dementia with Lewy bodies (DLB) and Parkinson disease (PD) are multifactorial.

59 emiologic data on dementia with Lewy bodies (DLB) and Parkinson disease dementia (PDD) remain limited

60 eding activity of dementia with Lewy bodies (DLB) and Parkinson's disease (PD) brain-derived alpha-sy

61 s associated with dementia with Lewy bodies (DLB) and Parkinson's disease (PD).

62 tive processes in dementia with Lewy bodies (DLB) and Parkinson's disease (PD).

63 r's disease (AD), dementia with Lewy bodies (DLB) and Parkinson's disease.

64 heimer's disease, dementia with Lewy bodies (DLB) and vascular cognitive impairment (VCI).

65 disease (PD) and dementia with Lewy bodies (DLB) are both characterized by the formation and intrane

66 disease (PD) and dementia with Lewy bodies (DLB) are both characterized pathologically by the presen

67 disease (PD) and dementia with Lewy bodies (DLB) are characterized by the presence of filamentous in

68 disease (PD) and dementia with Lewy bodies (DLB) are common neurodegenerative disorders of the aging

69 alyzed, including dementia with Lewy Bodies (DLB) as an additional control group.

70 emor and probable dementia with Lewy bodies (DLB) from Alzheimer disease.

71 n differentiating dementia with Lewy bodies (DLB) from Alzheimer's disease (AD) but it is not known h

72 mentia (FTD), and dementia with Lewy bodies (DLB) from normal aging and from each other and the relat

73 mentia (PDD), and dementia with Lewy bodies (DLB) has long been debated.

74 matory profile in dementia with Lewy bodies (DLB) has never before been investigated.

75 ic alterations in dementia with Lewy bodies (DLB) have been widely documented in postmortem studies,

76 atrophy (PCA) and dementia with Lewy bodies (DLB) have both been associated with occipital lobe hypom

77 ugh patients with dementia with Lewy bodies (DLB) have shorter disease duration than patients with Al

78 Dementia with Lewy Bodies (DLB) is a common neurodegenerative disorder with poor pr

79 Dementia with Lewy bodies (DLB) is recognised as the second most common form of dem

80 Dementia with Lewy bodies (DLB) is the second most common cause of degenerative dem

81 Dementia with Lewy bodies (DLB) is the underlying aetiology of 10-15% of all cases

82 Dementia with Lewy bodies (DLB) needs to be distinguished from other types of demen

83 nts with probable dementia with Lewy bodies (DLB) often have Alzheimer's disease (AD)-related patholo

84 ory impairment in dementia with Lewy bodies (DLB) remain unclear.

85 Patients who have dementia with Lewy bodies (DLB) show both clinical and histopathologic overlap with

86 D, respectively), dementia with Lewy bodies (DLB), and Alzheimer dementia (AD) traditionally have bee

87 mer disease (AD), dementia with Lewy bodies (DLB), and frontotemporal dementia (FTD).

88 n's disease (PD), dementia with Lewy bodies (DLB), and multiple system atrophy (MSA) are characterize

89 son disease (PD), dementia with Lewy bodies (DLB), and multiple system atrophy (MSA).

90 with dementia and dementia with Lewy bodies (DLB), are human neurodegenerative diseases(1).

91 heimer's disease, dementia with Lewy bodies (DLB), mixed Alzheimer's disease/DLB, frontotemporal loba

92 n's disease (PD), dementia with Lewy bodies (DLB), multiple system atrophy (MSA) and pure autonomic f

93 disease (AD) from Dementia with Lewy Bodies (DLB), on peptide level the hidden proteome contributed a

94 ilarities between dementia with Lewy bodies (DLB), Parkinson's and Alzheimer's diseases (PD and AD, r

95 ause of dementia, dementia with Lewy bodies (DLB), remains unclear.

96 disease (PD) and Dementia with Lewy Bodies (DLB).

97 he development of dementia with Lewy bodies (DLB).

98 disease (PD) and dementia with Lewy bodies (DLB).

99 disease (PD) and dementia with Lewy bodies (DLB).

100 disease (PD) and dementia with Lewy bodies (DLB).

101 disease (PD) and dementia with Lewy bodies (DLB).

102 ylation in PD and dementia with Lewy bodies (DLB).

103 ologies of AD and dementia with Lewy bodies (DLB).

104 s disease (PD) or dementia with Lewy bodies (DLB).

105 disease (PD) and dementia with Lewy bodies (DLB).

106 (PD, n = 16), and dementia with Lewy bodies (DLB, n = 13), and CON subjects (n = 15).

107 (PD, n = 1,013), dementia with Lewy bodies (DLB, n = 415), and control subjects (n = 6,155).

108 ase (PD, n = 39), dementia with Lewy bodies (DLB, n = 58), other neurodegenerative, vascular, or neur

109 (AD; n = 38) and dementia with Lewy bodies (DLB; n = 30) and controls (n = 30) underwent (18)F-FDG P

110 gation of AD from dementia with Lewy bodies (DLB; n = 34) was achieved with 90% sensitivity and speci

111 n disease, transgenic mice that develop both DLB and AD pathologies (DLB-AD mice) exhibit accelerated

112 e have shown for the first time that in both DLB and AD, increased peripheral inflammation occurs ear

113 he cingulate island sign was present in both DLB and PCA, although it was more asymmetric in PCA.

114 raphy have similar sensitivity for detecting DLB, but the latter appears to be more specific for excl

115 In patients with newly diagnosed DLB, symptoms are not associated with a reduction in str

116 123)I-PE2I) in patients with newly diagnosed DLB.

117 ow well the scan performs in differentiating DLB from frontotemporal dementia (FTD).

118 se (PD) and dementia with Lewy body disease (DLB).

119 among individuals with Alzheimer's disease, DLB and VCI.

120 DLB and those with mixed Alzheimer's disease/DLB and Alzheimer's disease pathology, and between those

121 zheimer's disease, mixed Alzheimer's disease/DLB and PSP groups, which all showed similar rates of at

122 se from cases with mixed Alzheimer's disease/DLB pathology, they demonstrate important pathophysiolog

123 VBSI than the DLB, mixed Alzheimer's disease/DLB, Alzheimer's disease and PSP groups, with a similar

124 Lewy bodies (DLB), mixed Alzheimer's disease/DLB, frontotemporal lobar degeneration with ubiquitin-on

125 zheimer's disease, mixed Alzheimer's disease/DLB, FTLD-U, CBD and PSP groups.

126 ue to be clinically useful in distinguishing DLB from Alzheimer's disease.

127 al test measures were compared for pure DLB, DLB+AD and pure AD using univariate analysis of covarian

128 stemic inflammatory mediators in established DLB and AD, as well as in their prodromal, mild cognitiv

129 ng to the imaging repository of the European DLB Consortium.

130 For DLB and PD-impaired patients, greater [18F]AV-1451 uptak

131 of the International Consensus Criteria for DLB has recommended that low DAT uptake in the basal gan

132 ent clinically based diagnostic criteria for DLB have limited accuracy.

133 the APOE is a strong genetic risk factor for DLB, confirming previous findings, and that the SNCA and

134 ns in GBA1 are a significant risk factor for DLB.

135 We report two susceptibility loci for DLB at genome-wide significance, providing insight into

136 values for healthy subjects, BPND values for DLB patients were significantly lower in the Ch4 termina

137 Four DLB patients with apathy and 4 DLB patients without apat

138 predictors of pure DLB from pure AD and from DLB+AD.

139 for distinguishing Alzheimer's disease from DLB and VCI in pathologically confirmed cases.

140 and in the striatum, distinguished PDD from DLB.

141 e also extracted low levels of beta-syn from DLB brains, but failed to extract any gamma-syn.

142 t delirium may be an early marker for future DLB, which would aid early diagnosis of DLB and identify

143 g 542 incident cases of parkinsonism, 64 had DLB and 46 had PDD.

144 However, DLB showed greater hypometabolism in the medial occipita

145 However, DLB+AD did not show significant neuropsychological diffe

146 enic mouse model recapitulates that in human DLB.

147 Objective: To contrast tau aggregation in DLB, cognitively impaired persons with PD (PD-impaired),

148 Peripheral inflammation is altered in DLB compared with AD, with T cell subset analysis suppor

149 of axonal damage in these mice as well as in DLB and PD.

150 y a signature pattern of cerebral atrophy in DLB and to compare it with the pattern found in Alzheime

151 T cells and reduced activation of B cells in DLB compared with AD.

152 inflammatory signature of serum cytokines in DLB.

153 est an atypical pattern of tau deposition in DLB.

154 cognitive and neuropsychiatric disorders in DLB patients.

155 Our results confirm the existence in DLB of cholinergic alterations, reaching both cortical a

156 n (IL)-1beta was detected more frequently in DLB and the serum concentration of IL-6 was increased co

157 romal DLB to assess if scores were higher in DLB compared to PD.

158 of this unique peripheral immunophenotype in DLB could guide development of an immune-based biomarker

159 n CA2 in the context of memory impairment in DLB.

160 studies examining peripheral inflammation in DLB using multiplex immunoassay and flow cytometry conco

161 striatal DAT despite its firm involvement in DLB pathology.

162 soluble alpha-synuclein protein are lower in DLB and PD, there is no evidence for a corresponding dec

163 ical test scores were significantly lower in DLB patients than in healthy subjects.

164 than DLB, and more reduction of midbrain in DLB than Alzheimer's disease.

165 striatal dopaminergic degeneration occurs in DLB, but not in Alzheimer's disease or most other dement

166 that although hippocampal Lewy pathology in DLB is predominant in CA2 and EC, memory performance cor

167 urodegeneration and clinical presentation in DLB patients.

168 a-synuclein seeding kinetics and products in DLB and PD indicated, for the first time, the existence

169 The basal ganglia, which play a key role in DLB, have also been implicated in delirium.

170 nt and fibrillary alpha-synuclein species in DLB-seeded reactions, whereas PD and control seeds faile

171 Damage to this network of structures in DLB may affect a number of different neurotransmitter sy

172 senescence of the adaptive immune system in DLB.

173 lcholine transporter, to evaluate in vivo in DLB the integrity of the 3 main cholinergic pathways-the

174 reof cause familial PD or dementia with LBs (DLB) in rare kindreds, but abnormal accumulations of wil

175 kinson's disease (PD) and dementia with LBs (DLB), are poorly understood.

176 ological diagnosis of pure DLB (n=12), mixed DLB and AD (DLB+AD n=23) and pure AD (n=89) who had Clin

177 to decreased (123) I-FP-CIT uptake in 7 non-DLB subjects (3 with concomitant parkinsonism) who had n

178 nly essential tremor), probable DLB, and non-DLB (mainly Alzheimer disease).

179 with specificity of 90.4% for excluding non-DLB dementia, which was predominantly due to Alzheimer's

180 ppears to be more specific for excluding non-DLB dementias, especially when parkinsonism is the only

181 robable (n=94) or possible (n=57) DLB or non-DLB dementia (n=147) established by a consensus panel (i

182 Notably, in our non-DLB group, myocardial imaging gave no false-positive rea

183 al diagnosis of DLB and 29 patients with non-DLB dementia (Alzheimer disease, n = 16; behavioral vari

184 The majority (9/10) of DLB cases had an abnormal scan and a significant reducti

185 tionship between the genetic architecture of DLB and other neurodegenerative disorders.

186 opathologically characterized human cases of DLB, finding that alpha-synuclein pathology was highest

187 implicated in PD or AD, in a large cohort of DLB cases and controls.

188 e major contributor to the memory deficit of DLB.

189 history of the condition; the definition of DLB; the relationship between DLB and other neurodegener

190 ded 30 patients with a clinical diagnosis of DLB and 29 patients with non-DLB dementia (Alzheimer dis

191 ture DLB, which would aid early diagnosis of DLB and identify those at high risk.

192 The mean age at diagnosis of DLB was earlier in GBA1 mutation carriers than in noncar

193 tics, clinical presentation and diagnosis of DLB; options for treatment; and potential future directi

194 B and this may aid in the differentiation of DLB from Alzheimer's disease.

195 even larger role in the genetic etiology of DLB than in PD, providing insight into the role of gluco

196 Delirium is a frequent presenting feature of DLB.

197 i.e., cingulate island sign) is a feature of DLB.

198 is study, we correlated the core features of DLB (dementia, parkinsonism, hallucinations, and fluctua

199 naptic pathologies are important features of DLB and PD, we sought to investigate the extent and char

200 to a number of the core clinical features of DLB.

201 The incidence of DLB increases steeply with age and is markedly higher in

202 Men had a higher incidence of DLB than women across the age spectrum.

203 EC --> CA2 circuitry in the pathogenesis of DLB symptoms.

204 lpha-syn are involved in the pathogenesis of DLB.

205 DLB, assess the association of phenotype of DLB with GBA mutations, and explore the effects of these

206 The incidence rate of DLB and PDD combined was 5.9.

207 The overall incidence rate of DLB is lower than the rate of Parkinson disease.

208 The incidence rate of DLB was 3.5 per 100,000 person-years overall, and it inc

209 parietal cortex is, therefore, suggestive of DLB and this may aid in the differentiation of DLB from

210 paired visuospatial function than pure AD or DLB+AD patients whereas memory function was more severel

211 ion was more severely impaired in pure AD or DLB+AD than in pure DLB.

212 o developed parkinsonism and, in particular, DLB or PDD from 1991 through 2005 (15 years).

213 ce that develop both DLB and AD pathologies (DLB-AD mice) exhibit accelerated cognitive decline assoc

214 covering disease modifying therapies for PD, DLB, and related synucleinopathies.

215 RBD, correlated with reduced survival in PD, DLB and MSA.

216 ry of disease modifying therapies for LB PD, DLB, and related neurodegenerative synucleinopathies.

217 ons from four groups of individuals with PD, DLB, Alzheimer's disease (AD) and matched controls.

218 RBD were compared with 207 patients with PD, DLB, or prodromal DLB to assess if scores were higher in

219 and progression of retinal pathology in a PD/DLB transgenic mouse model.

220 rates of motor and non-motor features of PD/DLB and of abnormal (123)I-ioflupane SPECTs.

221 ha-syn play a role in the pathogenesis of PD/DLB.

222 should be considered at increased risk of PD/DLB.

223 maging features associated with prodromal PD/DLB in patients with LOD.

224 t (E35K + E46K + E61K) that amplifies the PD/DLB-causing E46K mutation induced alphaS-rich vesicle cl

225 atients clinically characterized as PD, PDD, DLB, amnestic mild cognitive impairment, and AD.

226 (P=0.07), whereas patients classified as PDD/DLB by clinical follow-up did not (P=0.65).

227 with dementia/dementia with Lewy bodies (PDD/DLB) exhibited a trend toward shorter survival than thos

228 condary endpoints and a subgroup of possible DLB patients was also included.

229 ly diagnosed clinically probable or possible DLB underwent genotyping for the 7 known AJ GBA mutation

230 e GBA1 mutation carrier status as predicting DLB or PD with dementia status, using common control sub

231 een clinically diagnosed PCA and 13 probable DLB subjects underwent (18)F-FDG PET.

232 een clinically diagnosed PCA and 13 probable DLB subjects underwent (18)F-FDG PET.

233 ity of 77.7% for detecting clinical probable DLB, with specificity of 90.4% for excluding non-DLB dem

234 onsecutive patients with clinically probable DLB (n = 19) from the Mayo Clinic Alzheimer's Disease Re

235 hat fulfilled clinical criteria for probable DLB were age- and gender-matched to 72 patients with pro

236 take distinguishes AD dementia from probable DLB, which may be useful for differential diagnosis.

237 take distinguishes AD dementia from probable DLB, which may be useful for differential diagnosis.

238 tely distinguished AD dementia from probable DLB.

239 tal and occipital AV-1451 uptake in probable DLB and its association with global cortical PiB uptake

240 clinically normal controls, and in probable DLB, the uptake in these regions correlated with global

241 the ante-mortem differentiation of probable DLB from other causes of dementia, of single photon emis

242 T SPECT and a clinical diagnosis of probable DLB.

243 ntly higher AV-1451 uptake than the probable DLB group, and medial temporal uptake completely disting

244 , non-PS (mainly essential tremor), probable DLB, and non-DLB (mainly Alzheimer disease).

245 Patients with probable DLB had greater AV-1451 uptake in the posterior temporop

246 cer AV-1451 uptake in patients with probable DLB, compared to AD, and its relationship to beta-amyloi

247 s of clinical guideline criteria, a probable-DLB diagnosis at follow-up 16 +/- 11.6 mo later.

248 with 207 patients with PD, DLB, or prodromal DLB to assess if scores were higher in DLB compared to P

249 n some cases, represent early or 'prodromal' DLB.

250 is including only neuropathologically proven DLB cases (667 cases).

251 h LBDNCs and no or low levels of ADNCs (pure DLB [pDLB] group; n=91), Parkinson disease dementia (PDD

252 logical test measures were compared for pure DLB, DLB+AD and pure AD using univariate analysis of cov

253 uospatial function was more affected in pure DLB than in AD while memory retrieval deficit was more a

254 deficit was more affected in AD than in pure DLB, in the early stages of dementia.

255 y impaired in pure AD or DLB+AD than in pure DLB.

256 ed cases with pathological diagnosis of pure DLB (n=12), mixed DLB and AD (DLB+AD n=23) and pure AD (

257 clinical features of the early stage of pure DLB compared with AD.

258 ognition were independent predictors of pure DLB from pure AD and from DLB+AD.

259 The pure DLB patients showed more impaired visuospatial function

260 Before or on the day of the SPECT scan, DLB patients had a routine neurologic examination includ

261 onversion to a synucleinopathy, specifically DLB.

262 duction of SI GM in Alzheimer's disease than DLB, and more reduction of midbrain in DLB than Alzheime

263 e asymmetric patterns of hypometabolism than DLB.

264 These results indicate that DLB has a unique genetic risk profile when compared with

265 The DLB group showed very little cortical involvement on VBM

266 els of soluble oligomers of alpha-syn in the DLB brains compared to those with Alzheimer's disease an

267 However, atrophy rates in the DLB group were not significantly different from control

268 volved surrounding areas, as observed in the DLB group.

269 lobe and inferior temporal regions than the DLB group.

270 ich were both significantly greater than the DLB group.

271 ntly greater rates of BBSI and VBSI than the DLB, mixed Alzheimer's disease/DLB, Alzheimer's disease

272 with carriers of severe mutations closer to DLB than to idiopathic PD.

273 carriers of severe mutations were closer to DLB.

274 nterval [CI] = 1.053-4.803), specifically to DLB (OR = 4.754; 95% CI = 1.283-17.618, p = 0.020) and n

275 Overall, sensitivity and specificity to DLB were respectively 93% and 100% for (123) I-MIBG myoc

276 e relatively consistent across the variegate DLB spectrum.

277 (AUC = 0.93 vs. 0.72, P = 0.001) and AD vs. DLB (AUC = 0.80 vs. 0.58, P = 0.005) comparisons.

278 93 participants (31 with DLB, 31 with AD and 31 healthy older controls) completed

279 patterns of cerebral atrophy associated with DLB have not been well established.

280 ated common genetic variants associated with DLB in a large European multisite sample.

281 E epsilon4 (Chr19) loci were associated with DLB surpassing the genome-wide significance threshold (p

282 he p.N370S variant in GBA is associated with DLB, which, together with the findings at the SCARB2 loc

283 16q24.2), showed suggestive association with DLB at p-value < 1 x 10(-6).

284 pathologically well-characterized cases with DLB, PD, and controls (Ctrl).

285 of 91% and specificity of 94%) compared with DLB and VCI.

286 levance: One in 3 AJ patients diagnosed with DLB were carriers of a GBA mutation, making it the most

287 s of an AJ cohort of patients diagnosed with DLB, assess the association of phenotype of DLB with GBA

288 only observed at autopsy in individuals with DLB and PD dementia, but their contribution to these dis

289 th MSA differ from those of individuals with DLB, which suggests that distinct conformers or strains

290 atients with DLB (n=37), AD (n=20), MCI with DLB profile (n=38), MCI with AD profile (n=20) and healt

291 Results: Among the 35 patients with DLB (23 men [66%] and 12 women [34%]; mean [SD], 69.6 [8

292 e obtained plasma samples from patients with DLB (n=37), AD (n=20), MCI with DLB profile (n=38), MCI

293 ggregates of tau are common in patients with DLB and in PD-impaired patients, even in those without e

294 ilar to clinical and prodromal patients with DLB but higher scores compared with patients with PD.

295 ha-synuclein in the RT-QuIC in patients with DLB compared to PD and Ctrl.

296 Patients with DLB were younger at onset of symptoms than patients with

297 ower in 4 of the 5 regions for patients with DLB, and in 2 of the 5 regions for patients with PD, com

298 Results: In patients with DLB, cortical [18F]AV-1451 uptake was highly variable an

299 fluence disease duration among patients with DLB.

300 tant prognostic information to patients with DLB.