ライフサイエンスコーパス: DLB

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

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

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

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

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

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

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

8 The cohort comprised 788 DLB cases and 2624 controls.

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

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

11 ask (DLB < Alzheimer's disease P = 0.031 and DLB < control P = 0.048).

12 ation-matched patients with PDD (n = 20) and DLB (n = 20), Alzheimer's disease (n = 22) and Parkinson

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

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

15 ation in one AD patient revealed both AD and DLB changes despite the absence of clinical parkinsonism

16 alpha2A-AR mRNA in the hippocampus of AD and DLB subjects were not altered, but expression of alpha1D

17 d profound neuronal loss in the LC in AD and DLB subjects with three major changes in the noradrenerg

18 In AD and DLB subjects, the postsynaptic alpha1-ARs were normal to

19 Therefore, in AD and DLB subjects, there is compensation occurring in the rem

20 icantly reduced in the hippocampus of AD and DLB subjects.

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

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

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

24 ve disorders such as Parkinson's disease and DLB (dementia with Lewy bodies).

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

26 differences between Alzheimer's disease and DLB, reflecting the distribution of functional pathology

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

28 association between rare variants in GRN and DLB.

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

30 PCA and DLB showed overlapping patterns of hypometabolism involv

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

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

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

34 ngulate island sign differed between PCA and DLB.

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

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

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

38 ity of VH for Lewy-body parkinsonism (PD and DLB combined) was 92.9% (95% CI 89.1-95.8) and the posit

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

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

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

42 o cognitive impairment or dementia in PD and DLB.

43 rease in DNA methylation reported for PD and DLB.

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

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

46 PDD and DLB patients had similar impairment in all tasks (P > 0.

47 milarities in saccade performance in PDD and DLB underline the overlap between these conditions and u

48 and subcortical neurodegeneration in PDD and DLB.

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

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

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

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

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

54 flexive tasks allowed discrimination between DLB versus Alzheimer's disease (sensitivity > or =60%, s

55 ementia (PDD) and dementia with Lewy bodies (DLB) affect cortical and subcortical networks involved i

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

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

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

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

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

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

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 mer's disease and dementia with Lewy bodies (DLB) in resting occipital activity lead to activation di

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) needs to be distinguished from other types of demen

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

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

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

85 m sporadic PD and dementia with Lewy bodies (DLB) subjects was also examined.

86 20 patients with dementia with Lewy bodies (DLB), 25 with Alzheimer's disease (AD), and 19 normal el

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

88 73% (32/44) with dementia with Lewy bodies (DLB), and in only 7% (18/255) of patients with non-Lewy-

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

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

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

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

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

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

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

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

97 menting disorder, dementia with Lewy bodies (DLB).

98 (AD), and 20 had dementia with Lewy bodies (DLB).

99 organization, to dementia with Lewy bodies (DLB).

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

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

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

103 8), patients with dementia with Lewy bodies (DLB, n = 17) and control subjects (n = 36) were acquired

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

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

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

107 Both DLB groups had an anterior to posterior binding deficit

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

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

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

111 arkinsonism at least 1 year before dementia (DLB/PD) and 14 developed dementia before parkinsonism or

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

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

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

115 that PET with (+)-[(11)C]DTBZ differentiates DLB from AD, and decreased binding in AD may indicate su

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

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

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

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

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

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

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

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

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

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

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

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

128 free survival ranged from 62% to 73% for FCC/DLB, FCC/Fol, and MZ/MZ but was 33% for Leg/DLB (P =.6).

129 Five-year overall survival was 100% for FCC/DLB, FCC/Fol, and MZ/MZ but was 67% for Leg/DLB (P =.07)

130 y EORTC and diffuse large B-cell by WHO (FCC/DLB), 25% (eight of 32) follicle center cell by EORTC an

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

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

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

134 s by EORTC criteria satisfy WHO criteria for DLB lymphoma.

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

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

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

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

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

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

141 l electrophoresis of temporal neocortex from DLB patients but not from controls.

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

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

144 erns of task-related activity across groups, DLB patients showed more activation than Alzheimer patie

145 und for the face task (Alzheimer's disease > DLB P = 0.05; Alzheimer's disease > controls P = 0.14) a

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

147 However, DLB showed greater hypometabolism in the medial occipita

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

149 HR DLB-CLs also contained significantly higher numbers of m

150 enic mouse model recapitulates that in human DLB.

151 Reaction time or accuracy in DLB and Alzheimer's disease differed significantly from

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

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

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

155 est an atypical pattern of tau deposition in DLB.

156 cognitive and neuropsychiatric disorders in DLB patients.

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

158 increase in TH mRNA were somewhat greater in DLB subjects), the presence of Lewy bodies in addition t

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

160 striatal DAT despite its firm involvement in DLB pathology.

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

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

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

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

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

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

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

168 bodies in addition to plaques and tangles in DLB subjects does not appear to further affect the norad

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

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

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

172 /DLB, FCC/Fol, and MZ/MZ but was 67% for Leg/DLB (P =.07).

173 /DLB, FCC/Fol, and MZ/MZ but was 33% for Leg/DLB (P =.6).

174 y EORTC and diffuse large B-cell by WHO (Leg/DLB).

175 ol < Alzheimer's disease P = 0.02; control < DLB P = 0.019; motion: control < Alzheimer's disease P =

176 l < Alzheimer's disease P = 0.118; control < DLB P = 0.118) but could be accounted for by behavioural

177 s with Alzheimer's disease (n = 10; 5 male), DLB (n = 9; 4 male) and controls (n = 13; 5 male) perfor

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

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

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

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

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

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

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

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

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

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

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

189 e major contributor to the memory deficit of DLB.

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

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

195 Delirium is a frequent presenting feature of DLB.

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

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

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

199 clinical and neuropsychological features of DLB, providing a possible distinctive marker for this di

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 sures and memory tasks in the early stage of DLB.

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

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

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

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

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

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

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

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

220 etergent-insoluble fraction from sporadic PD/DLB brains, but are reduced in the insoluble fraction fr

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

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

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

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

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

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

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

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

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

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

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

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

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

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

235 tely distinguished AD dementia from probable DLB.

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

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

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

239 T SPECT and a clinical diagnosis of probable DLB.

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

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

242 were obtained from 15 patients with probable DLB and 10 sex- and age-matched healthy controls.

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

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

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

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

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

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

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

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

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

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

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

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

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

256 The pure DLB patients showed more impaired visuospatial function

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

258 Six DLB patients developed parkinsonism at least 1 year befo

259 eased binding in AD may indicate subclinical DLB pathology in addition to AD pathology.

260 the exception of accuracy in the face task (DLB < Alzheimer's disease; P = 0.038).

261 se > controls P = 0.14) and the motion task (DLB < Alzheimer's disease P = 0.031 and DLB < control P

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 he subcortical grey matter may indicate that DLB and Parkinson's disease share a similar nigrostriata

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

266 The DLB group showed very little cortical involvement on VBM

267 The DLB/AD group showed significant binding asymmetry only i

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

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

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

271 77% in the DLB/PD group and 45 to 67% in the DLB/AD compared to AD and control.

272 potential was decreased by 62 to 77% in the DLB/PD group and 45 to 67% in the DLB/AD compared to AD

273 Binding was lower in the DLB/PD group than the DLB/AD, but the differences reache

274 lobe and inferior temporal regions than the DLB group.

275 ich were both significantly greater than the DLB group.

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

277 nding was lower in the DLB/PD group than the DLB/AD, but the differences reached only marginal signif

278 fore parkinsonism or at about the same time (DLB/AD).

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

280 carriers of severe mutations were closer to DLB.

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

282 Unlike DLB lymphoma presenting in nodal or noncutaneous sites,

283 in these noradrenergic markers in AD versus DLB subjects were similar (except neuronal loss and the

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

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

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

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

288 fferences were observed in PDD compared with DLB.

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

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

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

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

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

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

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

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 tant prognostic information to patients with DLB.

300 fluence disease duration among patients with DLB.