ライフサイエンスコーパス: AD

1 AD domain analysis showed the AD domain of both ADADs wa

2 AD mice had more SWS, but reduced SWR density.

3 AD pathology is characterized by the accumulation of amy

4 33 participants were enrolled, including 13 AD(-)PA(+), 9 AD(+)PA(+), and 11 nonatopic (NA) particip

5 f the winter westerlies from 1810 until 1880 AD.

6 ography fractioned protein samples from 3xTg-AD mouse model brain homogenates.

7 ts were enrolled, including 13 AD(-)PA(+), 9 AD(+)PA(+), and 11 nonatopic (NA) participants.

8 ADpred identifies known acidic ADs within transcription factors and accurately predicts

9 ion using a genetic risk score (GRS) for AD (AD-GRS), in 406,536 UK Biobank participants with Europea

10 skin barrier of subjects with PA without AD (AD(-)PA(+)) has not been studied.

11 proteins expression in an independent adult AD cohort validated differential expression of STS PC1 p

12 dvent of disease-modifying therapies against AD is imperative.

13 Here, we show that nearly all AD-associated-genes are evolutionarily old and did not o

14 d USA identified five variant carriers among AD patients only.

15 We applied the method to an AD dataset consisting of histone acetylation, DNA methyl

16 ct candidate genes, applied the method to an AD dataset, and identified several disease-related genes

17 liative care (37% versus 27%, p = 0.002) and AD inclusion in hospital files (10% versus 3%, p < 0.001

18 nscriptome signatures among CTE, CTE/AD, and AD.

19 commonly down-regulated in CTE, CTE/AD, and AD.

20 ular senescence in the context of ageing and AD, and discusses which of the processes - cellular sene

21 reased use of specialist palliative care and AD inclusion in hospital files of intervention patients

22 ways associated with both binge drinkers and AD are also analyzed.

23 ariations existed in life cycle GWP, EU, and AD among counties and across years.

24 Over time, RD, FA, and AD values of the dorsal and lateral tracts on the injure

25 ciated with increased human-Abeta levels and AD pathology.

26 approaches to analyse the effect of MDD and AD on human AHN and analyse different studies implicatin

27 lt hippocampal neurogenesis (AHN) in MDD and AD.

28 a potential converging mechanism in MDD and AD.

29 he propagation of tau protein misfolding and AD pathogenesis, providing a new conceptual framework th

30 negative correlation exists between OAG and AD diagnosis.

31 ization (MR) to evaluate whether obesity and AD are causally interlinked.

32 is central to the association between PD and AD.

33 ies of the LEKTI domain 4 (D4) and D6 WT and AD-associated mutants on the enzyme activities of KLK5 a

34 Individuals clinically classified as AD dementia but having negative Abeta PET scans show lit

35 Between AD 800 and 1000 forest regrowth was evident, but this tr

36 roaches to investigate the crosstalk between AD and psychosis.

37 sal genes, 16 shared causal pathways between AD and T2DM, and 754 gene expression and 101 gene methyl

38 evident, but this trend was reversed between AD 1000 and 1200 as drier conditions coincided with rene

39 Similar effect sizes between AD and HC groups were obtained across the different imag

40 licated impaired glymphatic function in both AD and iNPH.

41 ethylation nodes that were connected to both AD and T2DM in multi-omics causal networks.

42 By AD 1230 forests had regrown in the valley and maize cult

43 ubiquitously expressed but are regulated by AD risk variants within myeloid enhancers in a cell type

44 Our data in cellular AD models indicates that increased levels of uncleaved C

45 sotho, directly dated to the seventh century AD at Likoaeng and the tenth century AD at the nearby si

46 century AD at Likoaeng and the tenth century AD at the nearby site of Sehonghong.

47 tion is impaired in preclinical and clinical AD while mature NGF degradation is enhanced.

48 pathway was grossly upregulated in clinical AD and significantly correlated with disease severity an

49 associated with the development of clinical AD; especially, the time-specific associations were nota

50 Nf-L and GFAP 4 to 8 years prior to clinical AD.

51 in subjects who were diagnosed with clinical AD during life and had a diagnosis of AD confirmed post-

52 and tau together are more suitable to combat AD than therapies against one or the other alone.

53 ant, stage III melanoma in the phase 3 COMBI-AD trial.

54 thermore, Prkcz null mice showed compromised AD-like phenotypes in the MC903 AD model.

55 ique transcriptome signatures among CTE, CTE/AD, and AD.

56 ns) were commonly down-regulated in CTE, CTE/AD, and AD.

57 recapitulated in a three-dimensional culture AD model, virus-infected APP/PS1 mice and the brains of

58 mary outcome parameter was arrhythmic death (AD) or resuscitated cardiac arrest (RCA).

59 7 differentiated neuropathologically defined AD from non-AD (area under the curve [AUC], 0.89 [95% CI

60 on (GReX) of ZC3H12B and Alzheimer dementia (AD) (p value = 5.42 x 10(-13)), neurofibrillary tangle d

61 ) and individuals with Alzheimer's dementia (AD).

62 mutations associated with atopic dermatitis (AD) affect the protease inhibitory activity of LEKTI or

63 Atopic dermatitis (AD) is a complex inflammatory disorder with multiple int

64 Atopic dermatitis (AD) is characterized by a skin barrier defect aggravated

65 transcriptome studies in atopic dermatitis (AD) showed broad dysregulation as well as "improvement"

66 young children with early atopic dermatitis (AD), but chronologic changes in the blood of infants and

67 or for the development of atopic dermatitis (AD), but several aspects of this association remain uncl

68 the skin of patients with atopic dermatitis (AD).

69 ins, and increased susceptibility to develop AD.

70 o identify individuals at risk of developing AD.

71 Tinnitus-related risk on developing AD/PD followingly was determined by the Cox regression t

72 ns of brain insulin signaling with diabetes, AD, and level of cognition.

73 Dry anaerobic digestion (AD) of organic municipal solid waste (MSW) followed by c

74 er-Hinton broth (ID-BMD), and agar dilution (AD) using standard Mueller-Hinton agar were performed ac

75 histological hallmark of Alzheimer disease (AD) and two dozen related neurodegenerative diseases.

76 Biomarker accuracy for Alzheimer disease (AD) is uncertain.

77 loid beta accumulation in Alzheimer disease (AD), but to the knowledge of the authors the association

78 sing physiologic model of Alzheimer disease (AD).

79 odegenerative diseases, Alzheimer's disease (AD) and Down syndrome (DS), using DNA methylation datase

80 diagnosis between FTLD, Alzheimer's disease (AD) and healthy ageing; their role as markers of disease

81 t plays a major role in Alzheimer's disease (AD) and other tauopathies.

82 egates is implicated in Alzheimer's disease (AD) and other tauopathies.

83 Tauopathies including Alzheimer's disease (AD) are marked by the accumulation of aberrantly modifie

84 Alzheimer's disease (AD) causes unrelenting, progressive cognitive impairment

85 ns with a connection to Alzheimer's disease (AD) demonstrated an association between increased levels

86 een viral infection and Alzheimer's disease (AD) has long been an area of interest, but proving causa

87 ly cognitive markers of Alzheimer's disease (AD) is becoming increasingly important.

88 Alzheimer's disease (AD) is characterized by amyloid plaques and progressive

89 es and tau pathology in Alzheimer's disease (AD) is not fully understood.

90 ve impairment (MCI) and Alzheimer's disease (AD) is poorly understood, particularly at early stages p

91 Alzheimer's disease (AD) is the most common age-related form of dementia, ass

92 Alzheimer's disease (AD) is the most common neurodegenerative disorder, resul

93 o neuroinflammation and Alzheimer's disease (AD) pathogenesis.

94 cancer development and Alzheimer's disease (AD) pathogenesis.

95 vascular dysfunction in Alzheimer's disease (AD) patients.

96 pathogen" hypothesis of Alzheimer's disease (AD) proposes that brain HSV-1 infection could be an init

97 sive disorder (MDD) and Alzheimer's disease (AD) reciprocally elevate the risk for one another.

98 Patients with Alzheimer's disease (AD) suffer from spatial memory impairment and wandering

99 n the brains tissues of Alzheimer's disease (AD), amyotrophic lateral sclerosis (ALS) and frontotempo

100 ween sleep duration and Alzheimer's disease (AD), but it is unclear if sleep duration is a manifestat

101 shown to be elevated in Alzheimer's disease (AD), but the impact of the directly measured iron on the

102 In Alzheimer's disease (AD), human Tau is phosphorylated at S199 (hTau-S199-P) b

103 However, in Alzheimer's disease (AD), its reflection on regional neuronal injury in the c

104 plays a central role in Alzheimer's disease (AD), since it drives the cognitive decline.

105 re-symptomatic stage of Alzheimer's disease (AD).

106 in SCZ and pathology in Alzheimer's disease (AD).

107 lism and progression of Alzheimer's disease (AD).

108 cular disease (CVD) and Alzheimer's disease (AD).

109 human brain proteome of Alzheimer's disease (AD).

110 nchyma are hallmarks of Alzheimer's disease (AD).

111 y complex diseases like Alzheimer's disease (AD).

112 tive diseases including Alzheimer's disease (AD).

113 se neurodegeneration in Alzheimer's disease (AD).

114 in the early stages of Alzheimer's disease (AD).

115 ogy during the onset of Alzheimer's disease (AD).

116 nset and progression of Alzheimer's disease (AD).

117 pmental disorder (PDD) or autistic disorder (AD) according to International Classification of Disease

118 enes reported to harbour autosomal dominant (AD) and recessive (AR) causative variants.

119 o therapy is available to block or slow down AD progression, and the mechanisms of the disease are no

120 sses that may be at play during the earliest AD-related immune response.

121 dentification of unique biomarkers for early AD.

122 S aureus is known to exacerbate AD, whereas S epidermidis has been considered a benefici

123 previous reports showing obesity exacerbates AD-related pathology and symptoms in mice.

124 investigators to develop models of familial AD by overexpressing human genes such as those encoding

125 O) cells and fibroblasts from PSEN1 familial AD patients, which restores lysosomal proteolysis, calci

126 .16] for ASD and 0.91 [CI, 0.70 to 1.18] for AD).

127 ith an RR of 6.56 (95% CI: 4.92 to 8.77) for AD.

128 ss rather than inflammation was critical for AD progression in this mouse model, and that disease pro

129 e is the most common genetic risk factor for AD and is related to a pro-inflammatory state.

130 y history of AD was a strong risk factor for AD.

131 uration using a genetic risk score (GRS) for AD (AD-GRS), in 406,536 UK Biobank participants with Eur

132 m propensity, has important implications for AD.

133 e differentiation of Th2 cells important for AD pathogenesis.

134 establishing prophylactic interventions for AD on a general population level.

135 We studied whether genetic liability for AD predicts sleep duration using a genetic risk score (G

136 early-stage biomarkers in those at risk for AD and age-related cognitive decline (ARCD) in order to

137 g blood-based biomarker that is specific for AD, correlates with cerebral Abeta and tau pathology, an

138 nt neuronal necrosis represents a target for AD therapeutics.

139 -invasive diagnostic and prognostic tool for AD, regardless of clinical stage, which would be of grea

140 fety and efficacy of systemic treatments for AD up to February 2020.

141 ity with a mean follow-up of 10-11 years for AD and all-cause dementia incidence.

142 Cerebral organoids from AD patients carrying APOE epsilon4/epsilon4 show greater

143 f-identified black race and progression from AD to asthma.

144 Further, AD-associated hyperphosphorylation of eukaryotic elongat

145 microglia-like cell lines (hMGLs) harboring AD variants in CD33, INPP5D, SORL1, and TREM2 loci and c

146 tifying none-to-low vs. intermediate-to-high AD neuropathologic change (ADNC) was assessed for all bi

147 ium arboreum (A(2)) and Gossypium hirsutum ((AD)(1)) genomes, we showed that all existing A-genomes m

148 However, little is known about how AD risk genes impact synaptic function.

149 gates extracted from cell cultures and human AD brain tissues, demonstrating the ability of the Hsp70

150 ) in mouse AD models and genome-edited human AD iPS cell-derived neurons.

151 ardiac and musculoskeletal deficits in human AD.

152 AD with many of the major hallmarks of human AD.

153 na, emphasizing an important role of 5hmC in AD pathogenesis and highlighting both ethnicity-specific

154 g against the pathologic actions of Abeta in AD.SIGNIFICANCE STATEMENT Elevated levels of beta-amyloi

155 arallel to its intracellular accumulation in AD, tau is also released in the extracellular space, as

156 trations in CSF and plasma are associated in AD-vulnerable regions in the presence of amyloid positiv

157 tissue, increases pro-oxidant iron burden in AD.

158 elucidate the precise role of iNKT cells in AD development of NC mice, we employed two distinct muri

159 ific enhancers, implicating myeloid cells in AD etiology.

160 IM32 ratio was associated with CD4+ cells in AD human skin compared with those in healthy controls.

161 vironmental factors and lifestyle choices in AD pathogenesis.

162 ritability and environmental contribution in AD in Taiwan.

163 important role in cerebrovascular damage in AD, we investigated the role of the Abeta-fibrinogen int

164 thological correlate to cognitive decline in AD.

165 unity to investigate therapeutic delivery in AD and other conditions.

166 HSV-1 DNA has been detected in AD amyloid plaques in human brains, and treatment with t

167 are considered the main pathogenic entity in AD, as compared to rodent Abeta, the rat Amyloid Precurs

168 3 and 5390 genes differentially expressed in AD and psoriasis lesions versus in controls, respectivel

169 x interactions among contributing factors in AD and the implications on disease development and thera

170 evation and oxidative burden that feature in AD pathology.

171 However, in AD mice, SWR-DW and spindle-DW coupling were impaired.

172 lapping changes of brain hydroxymethylome in AD.

173 1, and TREM2, well known genes implicated in AD by previous brain and genetic studies, in humans and

174 embers of this MMP family were implicated in AD neuropathology.

175 provided rapid and sustained improvements in AD symptoms and was well tolerated.

176 exhibited a concordant trend of increase in AD plasma in comparison with age-matched control plasma.

177 the ongoing microgliosis and synapse loss in AD models.

178 their diagnostic accuracy was only modest in AD patients.

179 nd microgliosis are consistently observed in AD transgenic animal models devoid of such pathologies,

180 erm usefulness of rupatadine for pruritus in AD.

181 to a T(H)2 cell-dominated immune response in AD are not completely understood.

182 mprehensive understanding of APOE4's role in AD pathogenesis, we performed a transcriptomics analysis

183 tau in driving neuronal dysfunction seen in AD.

184 Sensitivity at 95% specificity in AD participants was lower than in ED participants for cp

185 18)F-FDG uptake and mean (18)F-AV-45 SUVr in AD-typical regions were also significantly associated wi

186 us evidence in the field implicating them in AD.

187 nd, to investigate endogenous opioid tone in AD for the first time.

188 l disease (Pd), and infections with incident AD and all-cause dementia, among older adults (>=65 year

189 occurring and colorectal distension-induced AD.

190 adjuvant, the gB ectodomain protein (lacking AD-3) with squalene adjuvant, or lipid nanoparticle (LNP

191 Lesional AD skin shows a NK-cell dysregulation, which despite cli

192 ferentially expressed genes/DEGs in lesional AD and 662 DEGs in nonlesional AD, vs healthy skin (fold

193 CLDN8) genes were primarily seen in lesional AD.

194 tment of various neurological disorders like AD, PD, schizophrenia, epilepsy, brain cancer, CNS infec

195 compromised AD-like phenotypes in the MC903 AD model.

196 The performance of mean AD was comparable to that of radiobiologic dose metrics

197 RNA-sequencing from post-mortem AD human brains shows downregulation in the expression o

198 ility of endoplasmic reticulum (ER) in mouse AD models and genome-edited human AD iPS cell-derived ne

199 MRI volumes to test for there being multiple AD phenotypes.

200 RI were highly sensitive for neuropathologic AD.

201 elevated in those who progress to AD and non-AD dementias.

202 ated neuropathologically defined AD from non-AD (area under the curve [AUC], 0.89 [95% CI, 0.81-0.97]

203 onverted to AD dementia, or converted to non-AD dementias, and in cognitively unimpaired participants

204 rrier signatures in lesional and nonlesional AD and psoriasis skin, suggesting their utility as a min

205 s in lesional AD and 662 DEGs in nonlesional AD, vs healthy skin (fold-change >=2, FDR <0.05), with 1

206 id not originate later in evolution than not-AD-associated-genes.

207 Presence/absence of AD-like pathology was donor-specific (reproducible betwe

208 ET/MRI with hippocampal subfield analysis of AD, mild cognitive impairment (MCI), and healthy subject

209 utility as an easily accessible biomarker of AD pathology.

210 zed with intracellular Abeta in the brain of AD patients.

211 hydroxymethylation of the frontal cortex of AD patients from China, emphasizing an important role of

212 KLK7 was dispensable for the development of AD-associated skin inflammation.

213 inical AD during life and had a diagnosis of AD confirmed post-mortem by standardized criteria.

214 ential critical mechanism in the etiology of AD.

215 uccessfully predicted the daily evolution of AD severity scores at an individual level and could info

216 The exRNAs of AD-activated genes and transposons in the brain exhibite

217 H(2)O(2)(-)-induced pathological features of AD in GiDs are consistently recapitulated in a three-dim

218 k in the vicinity of pathogenic hallmarks of AD and other brain diseases.

219 The heritability of AD was estimated to be 57.0% for genetic factors, and 3.

220 to evaluate the effect of family history of AD on the incidence and prognosis of AD and estimate the

221 A family history of AD was a strong risk factor for AD.

222 r bicuspid aortic valve, a family history of AD was associated with an RR of 6.56 (95% CI: 4.92 to 8.

223 Effective management of AD requires a multipronged approach, not only restoring

224 Plasma NT1 tau is a specific marker of AD, which is elevated early in disease and may prove use

225 t sleep duration might be an early marker of AD.

226 alue = 1.89 x 10(-6)), and global measure of AD pathology (p value = 9.59 x 10(-7)).

227 e cellular and proteomic microenvironment of AD.

228 e synaptic plasticity in this mouse model of AD (P = 0.007 to untreated APP/PS1).

229 rt, and liver proteins from a mouse model of AD.

230 one and apomorphine were active in models of AD and PD.

231 vascular function in several mouse models of AD, including the J20-hAPP mouse.

232 significantly associated with lower odds of AD diagnosis.

233 a fibrillization to investigate the onset of AD over a long timescale.

234 mpact the neuropathology and pathogenesis of AD.

235 precise role of GR in the pathophysiology of AD remains unclear.

236 tory of AD on the incidence and prognosis of AD and estimate the heritability and environmental contr

237 proaches for slowing clinical progression of AD.

238 oration upon the underlying proteinopathy of AD, possibly by inducing oxidative stress or ferroptotic

239 f CCL2 are associated with increased risk of AD development as well as other inflammatory diseases.

240 role in memory decline in the early stage of AD.

241 ross the preclinical and prodromal stages of AD.

242 ion alterations may improve understanding of AD pathogenesis and lead to new biomarkers and treatment

243 ve advanced the mechanistic understanding of AD, single cell-based molecular alterations are largely

244 review progress and challenges in the use of AD mouse models, highlight emerging scientific innovatio

245 For many years, the prevailing view of AD pathogenesis has been that changes in Abeta precipita

246 meta-analysis also confirmed a DBP effect on AD (beta(GSMR) = -0.14, p = .03).

247 N2) carrying mutations linked to early-onset AD.

248 ed HR [aHR], 0.95 [95% CI, 0.81 to 1.12]) or AD (aHR, 0.96 [CI, 0.80 to 1.16]).

249 occurring vasomotion in patients with CAA or AD may be a promising early therapeutic option for preve

250 ch of the processes - cellular senescence or AD - might come first.

251 olycomb repressive complex 2 in pathological AD.

252 transcriptomic profiling in early pediatric AD is lacking.

253 th resulted in spontaneous, highly penetrant AD with many of the major hallmarks of human AD.

254 mposting nitrogen-rich organic waste or post-AD solids.

255 ipheral signatures associated with prevalent AD arising from lipid pathways including; ether lipids,

256 Efficacy outcomes regarding AD, PAR and PAA were collected at baseline and 16 weeks.

257 tly: Eczema Area and Severity Index, SCOring AD, Patient-Oriented Eczema Measure, pruritus score, sle

258 esional) with early-onset moderate-to-severe AD (<=6 months) and 17 healthy controls.

259 serum samples from 146 patients with severe AD (median Eczema Area and Severity Index = 28.3; interq

260 udy examined the role of two testis-specific AD domain proteins, ADAD1 and ADAD2, on testis RNA editi

261 and GFAP predict the development of sporadic AD and cognitive decline, and changes in structural brai

262 h effects likely contribute to its sustained AD-like activity.

263 epigenomic annotations has demonstrated that AD risk variants are enriched in myeloid-specific enhanc

264 The AD-AE model consists of two neural networks: (i) an auto

265 k effect on the sulfidation of Fe during the AD process.

266 study with a total of 857 subjects from the AD (n = 213), MCI (n = 322), and control (CN, n = 322) g

267 in the presence of amyloid positivity in the AD clinical spectrum and amyloid Tg rat model.

268 l changes in R2* values and cognition in the AD group.

269 if sleep duration is a manifestation of the AD disease process.

270 as reported to block the accumulation of the AD-associated proteins beta-amyloid (Abeta) and hyper-ph

271 is an early event in the development of the AD-like pathology and cognitive decline in DS, and for t

272 AD domain analysis showed the AD domain of both ADADs was likely catalytically inactiv

273 Several of these AD risk genes are specifically expressed in myeloid cell

274 ho remained cognitively stable, converted to AD dementia, or converted to non-AD dementias, and in co

275 sma NfL is elevated in those who progress to AD and non-AD dementias.

276 ays, is elevated in subjects who progress to AD dementia.

277 HHV-6 demonstrated little specificity to AD brains over controls by either method, whereas other

278 there were 193 ADRD events of which 158 were AD.

279 0.80 [0.74,0.86], P < .001; current wheeze, AD and rhinitis).

280 In this study, we test whether AD pathogenesis is associated with dysregulation in brai

281 ith other structural brain features and with AD and schizophrenia.

282 e modules most significantly associated with AD pathology and cognitive impairment.

283 act with dogs, was inversely associated with AD risk (OR = 0.40; P-value = .004).

284 toxic stimulation, have been associated with AD.

285 es in the blood of infants and children with AD through adolescence have not been explored.

286 cpCD was higher for ED (0.95) compared with AD (0.68) patients (P < 0.001).

287 ower cpCD was found in ED eyes compared with AD eyes in mild glaucoma (mean, 42.2% [95% confidence in

288 ities in the brains of persons who died with AD suggest that this reduction is the main cause for the

289 s and pathological extracts from donors with AD and chronic traumatic encephalopathy.

290 t with the possibility that individuals with AD, much like people with cancer, may have multiple mole

291 samples were obtained from 61 patients with AD (20 with mild or limited disease, 17 with moderate di

292 SFCT was similar among patients with AD and MCI and control subjects on multivariable analysi

293 s times (CLTs) were shorter in patients with AD but comparable to controls in patients with ACLF.

294 ocampal NLGN1 was decreased in patients with AD in comparison to patients with mild cognitive impairm

295 proteins in the skin of adult patients with AD with the history of clinical reactions to peanut.

296 ng the loss of bone density in patients with AD, paralleling the increase in fracture and fall risk i

297 laques in postmortem brains of patients with AD.

298 APP/PS1 mice and the brains of patients with AD.

299 consistent differences between persons with AD and controls.

300 The skin barrier of subjects with PA without AD (AD(-)PA(+)) has not been studied.