ライフサイエンスコーパス: AD

1 AD is a heterogeneous disease both clinically and biolog

2 AD-LIBS correctly infers 87-91% of ancestry in simulatio

3 AD-LIBS is an effective tool for ancestry inference that

4 AD-LIBS is therefore likely to be useful in studies of n

5 AD-related cellular dysfunctions have been linked to thi

6 om the volar forearms of 10 CSU patients, 10 AD patients, and 10 healthy normal controls (NCs) and me

7 After 1800 AD, there are rapid increases in (15)N enrichment in the

8 ively constant values from 1250 BC to 1800 AD.

9 plotypes and AD risk in 309 individuals (191 AD, 118 cognitively normal [CN] controls) from the San F

10 y a change in phosphate source rocks in 1998 AD, and a corresponding shift in fertilizer isotope comp

11 lasma samples from patients with DLB (n=37), AD (n=20), MCI with DLB profile (n=38), MCI with AD prof

12 replicated in brain slice cultures from 3xTg-AD mice.

13 een 1999-2015) and 11,381 individuals (5,728 AD, 5,653 CN controls) from the Alzheimer's Disease Gene

14 y SRPK2 plays a critical role in aggravating AD pathogenesis.

15 alue and identified almost all cases of aMCI/AD.

16 tion to the assessment of patients with aMCI/AD.

17 and suicidal ideation are more common among AD individuals, but do not lead to psychiatric consultat

18 summary, we show here that Rap1 contains an AD required for Rap1-dependent gene transcription.

19 gy coupled with cognitive improvements in an AD APP/PS1 transgenic mouse model.

20 sal degeneration is distinct from that of an AD patient.

21 ted by delta(15)N values at AD 1848-1852 and AD 1880-1930 correspond to the positive phase of the NAO

22 thods and across the 3 groups (YHV, AHV, and AD).

23 association between depression, anxiety, and AD in adults and examine the risk of hospitalization and

24 nts have a high risk of post-KT dementia and AD, and these sequelae associate with a profound effect

25 ssing contributing to barrier disruption and AD, and therefore we present novel therapeutic targets f

26 The BC half and AD half are available in five and eight steps, respectiv

27 the relationship between HLA haplotypes and AD risk in 309 individuals (191 AD, 118 cognitively norm

28 dominant secreted factor (in laboratory and AD clinical strains of S. aureus) inducing barrier integ

29 sceptibility contributes modestly to MDD and AD comorbidity.

30 , using summary data from the largest RA and AD Genome Wide Association (GWA) and meta-analysis studi

31 The causal relationship between RA and AD was assessed using Mendelian Randomization (MR), usin

32 c inflammatory rheumatoid arthritis (RA) and AD.

33 Conclusion DRLs and ADs as a function of patient size were developed for the

34 The risk of any AD and several individual ADs was consistently higher am

35 ncology or rheumatology, we have to approach AD in a more differentiated way (ie, to dissect and stra

36 d-beta-clearing capabilities with age and as AD progresses.

37 conditions indicated by delta(15)N values at AD 1848-1852 and AD 1880-1930 correspond to the positive

38 n mainland China, safety for TEVAR of type B AD appeared better between 2008 and 2015 than in previou

39 data (2006-2013) on acute complicated type B AD, stroke, paraplegia, in-hospital mortality and follow

40 ars, and acute (70%) or chronic (30%) type B AD.

41 We analyzed the association between AD PRSs and brain imaging parameters using T1-weighted s

42 No differences were found between AD and MCI subjects in BDNF levels (11 studies, Hedges'

43 quency of negative phases of the NAO between AD 1940-1975 is contemporaneous with higher delta(15)N v

44 The results suggest a familial link between ADs in general (that is, not limited to Streptococcus-re

45 moderate to severe PS, 10 subjects with both AD and CD, and 10 HC with no history of skin disease was

46 ether circulating Abeta contributes to brain AD-type pathologies remains largely unknown.

47 sieves) of a dihydrodipyrrin-carboxaldehyde (AD half) and a dihydrodipyrrin substituted with a beta-k

48 33 (G), within the previously reported CELF1 AD risk locus, showed association with delayed AD onset

49 Experimental systems for new-onset/chronic AD are needed to support rapid therapeutic development,

50 eristics of children with AD, ADHD, comorbid AD/ADHD and age-matched healthy controls and to investig

51 study analyzed criterion counts of comorbid AD and MD in African American and European American data

52 ance imaging (n = 829) to assess a composite AD signature cortical thickness and hippocampal volume (

53 nsitizations among patients with concomitant AD and ACD.

54 Current AD biomarkers are expensive and/or invasive and therefor

55 affect the expression of a number of defined AD-related targets.

56 risk locus, showed association with delayed AD onset and lower expression of SPI1 in monocytes and m

57 normal aging to Alzheimer disease dementia (AD) has also been observed.

58 evant association between atopic dermatitis (AD) and attention-deficit/hyperactivity disorder (ADHD).

59 Atopic dermatitis (AD) is a paradigmatic chronic inflammatory skin disease

60 Atopic dermatitis (AD), the most common chronic inflammatory skin disease,

61 ication of individuals at risk of developing AD and/or early stage AD for which current therapies may

62 ongly impact the lifetime risk of developing AD.

63 sed a question regarding physician-diagnosed AD and 2 versions of the UK Working Party Diagnostic Cri

64 Ps in Ireland which use anaerobic digestion (AD), thermal drying (TD), or lime stabilization (LS) tre

65 BMD), macrodilution (MD), and agar dilution (AD) methods were compared.

66 Alzheimer disease (AD) is a progressive disorder that affects cognitive fun

67 e clinical progression of Alzheimer disease (AD) is associated with the accumulation of tau neurofibr

68 ls at risk for developing Alzheimer disease (AD) is of utmost importance.

69 The metabolic basis of Alzheimer disease (AD) pathology and expression of AD symptoms is poorly un

70 cant event that underpins Alzheimer disease (AD) pathology.

71 healthy control (HC) and Alzheimer disease (AD) subjects, using reference region analyses.

72 2 pathologic hallmarks of Alzheimer disease (AD), and the spatial distribution of Abeta has been stud

73 ng appears in preclinical Alzheimer disease (AD), progresses with AD progression, and is associated w

74 ng how risk factors for Alzheimer's disease (AD) affect brain function and cognition in healthy adult

75 hin axonal swellings at Alzheimer's disease (AD) amyloid plaques.

76 Tauopathies, including Alzheimer's disease (AD) and other neurodegenerative conditions, are defined

77 l modification (PTM) in Alzheimer's disease (AD) and related tauopathies.

78 op post-KT dementia and Alzheimer's disease (AD) associated with their long-standing kidney disease a

79 iomarker present in the Alzheimer's disease (AD) brain is crucial for both clinical diagnosis and mon

80 ival analysis of 14,406 Alzheimer's disease (AD) cases and 25,849 controls identified eight previousl

81 n is fast increasing in Alzheimer's disease (AD) diagnosis.

82 thological hallmarks of Alzheimer's disease (AD) include amyloid-beta (Abeta) plaques, neurofibrillar

83 Alzheimer's disease (AD) is a detrimental neurodegenerative disease with no e

84 Alzheimer's disease (AD) is characterized by progressive cognitive decline, i

85 Alzheimer's disease (AD) is the most common form of dementia.

86 mportant contributor to Alzheimer's disease (AD) pathogenesis, as underscored by the recent identific

87 of canola oil intake on Alzheimer's disease (AD) pathogenesis.

88 eciated for its role in Alzheimer's disease (AD) pathology.

89 (Abetao) in triggering Alzheimer's disease (AD) pathophysiology.

90 e overrepresented in an Alzheimer's disease (AD) pathway.

91 egulated in PTSD and in Alzheimer's disease (AD) patients.

92 brain inflammation, in Alzheimer's disease (AD) progression.

93 eterogeneity underlying Alzheimer's disease (AD) requires a deep understanding of mechanisms affectin

94 Early intervention in Alzheimer's Disease (AD) requires novel biomarkers that can capture changes i

95 brains of patients with Alzheimer's disease (AD), and its expression levels influence the onset of th

96 genetic risk factor for Alzheimer's disease (AD), ApoE3 is neutral, and ApoE2 is protective.

97 disorders, such as the Alzheimer's Disease (AD), are associated with a marked drop in the levels of

98 nd late Braak stages of Alzheimer's disease (AD), as well as in other neurodegenerative disorders.

99 in the pathogenesis of Alzheimer's disease (AD), but little is known about the proteoforms present i

100 be the earliest sign of Alzheimer's disease (AD), it also occurs in aging and various neurological, m

101 ay an important role in Alzheimer's disease (AD).

102 ed pathologies, such as Alzheimer's disease (AD).

103 the pathophysiology of Alzheimer's disease (AD).

104 tients with early-stage Alzheimer's disease (AD).

105 thological hallmarks of Alzheimer's disease (AD).

106 ought to be affected in Alzheimer's disease (AD).

107 tial pathogenic role in Alzheimer s disease (AD).

108 ta and tau pathology in Alzheimer's disease (AD).

109 rain and degenerates in Alzheimer's disease (AD).

110 ate in individuals with Alzheimer's disease (AD).

111 ological diseases, like Alzheimer's disease (AD).

112 a signature feature of Alzheimer's disease (AD).

113 les of a mouse model of Alzheimer's disease (AD).

114 ative disorders such as Alzheimer's disease (AD).

115 Alzheimer's disease (AD; n = 164) was identified with 70% sensitivity and spe

116 ting scales can be used to identify distinct AD subtypes.

117 of the transcription factors Ascl1 and Dlx2 (AD) induces the generation of exclusively GABAergic neur

118 oid-beta (Abeta) and tau in the brain during AD, and islet amyloid polypeptide (IAPP) in pancreatic i

119 in the precuneus, a salient region for early AD changes.

120 are altered in pediatric patients with early AD, but T cells predominate in skin lesions.

121 role of PrP(C) to rescue or halt established AD endophenotypes in a therapeutic disease-modifying tim

122 trongly binds to the same MED25 site as ETV4 AD and JUN interacts with the other two MED25 sites.

123 ll-known inflammation inducer and a familial AD mutation.

124 or protein (hAPP mice), a model for familial AD that produces high brain levels of Abeta.

125 Finally, as predicted for a bona fide AD, mutation of this newly identified AD reduced the eff

126 by RD2 treatment may be also beneficial for AD patients.

127 d with a significant genetic risk factor for AD, changes in modulation may provide additional informa

128 n of immune-related genetic risk factors for AD, including coding variants in the gene TREM2 (trigger

129 r growing understanding of the mechanism for AD and is particularly focused on suppressing the skewed

130 hy individuals who are at increased risk for AD in the precuneus, a salient region for early AD chang

131 potential for targeting the APP673 site for AD drug development.

132 uld be an effective therapeutic strategy for AD.

133 stablishes ErbB2 as a therapeutic target for AD.

134 Inositol (SI) is a potential therapeutic for AD by directly interacting with the Abeta peptide to inh

135 potential use of TNF-targeted therapies for AD.

136 rm control but have never been validated for AD.

137 eline and follow-up, patient-reported global AD severity significantly correlated with oSCORAD (Spear

138 to cognitive status (normocognitive > MCI > AD; P < 0.0001).

139 Despite this high degree of heterogeneity, AD is still considered a single disease and usually trea

140 e highest PHS percentiles showed the highest AD incidence rates.

141 ggregates, which are characteristic of human AD and related tauopathies.

142 larly since animal models representing human AD are lacking.

143 a fide AD, mutation of this newly identified AD reduced the efficiency of Rap1 binding to a known tra

144 In AD, the translocator protein 18 kDa (TSPO) is overexpres

145 p (P = 0.007) and miR-4668-5p (P = 0.016) in AD patients compared with healthy controls.

146 am factors contributing to p53 activation in AD are not well understood.

147 selection is critical for amyloidogenesis in AD pathogenesis, and implicate a pharmaceutical potentia

148 r results emphasize the importance of APP in AD and should stimulate new studies to elucidate APP-rel

149 offer potential as a therapeutic approach in AD.

150 normal stratum corneum lipid architecture in AD and IV HEEs, independent of FLG genotype.

151 ential role for the IL-17A signaling axis in AD pathogenesis.

152 reactivation of latent HSV1 in the brain in AD pathogenesis are also discussed.

153 e mechanism underlying lysosomal deficits in AD remains poorly understood.

154 levels and attenuating synaptic deficits in AD.SIGNIFICANCE STATEMENT beta-Site amyloid precursor pr

155 atory pathways showed stronger enrichment in AD than psoriasis.

156 s, and anti-amyloid therapies in general, in AD treatment.

157 Although type 2 responses are implicated in AD, emerging evidence indicates a potential role for the

158 ch has been shown recently to be involved in AD pathology.

159 TERPRETATIONS: PPP4R3A is a gene involved in AD risk and progression.

160 ion could compromise the function of LSD1 in AD and FTD."LSD1 is a histone demethylase that plays man

161 PDE4D inhibitor is able to enhance memory in AD transgenic mice and concomitantly rescues their hippo

162 phorylation and subsequent neuropathology in AD and related tauopathies.

163 liorating effects of AD symptoms observed in AD/TTR(+/-) animal models after IDIF treatment and event

164 r gains of PRPH that were overrepresented in AD.

165 le is known about the proteoforms present in AD brain.

166 ) continues to dominate clinical research in AD, a deeper understanding of Abeta physiology has led t

167 athways were found to have a crucial role in AD pathogenesis.

168 (CK1epsilon) was increased significantly in AD brains.

169 d CAD cases but was reduced significantly in AD.

170 Few studies in AD have tested hypotheses regarding which medication wil

171 mmation and a possible therapeutic target in AD and psoriasis.

172 We provide evidence that increased AD risk may be at least partly mediated by deficient mic

173 The risk of any AD and several individual ADs was consistently higher among first-degree relatives

174 , in mouse models of spontaneous and induced AD-like lesions, there was delayed re-epithelialization.

175 rate Abeta, leading to recessively inherited AD.

176 chnology could robustly detect intracellular AD-related protein changes caused by a well-known inflam

177 , placebo-controlled, phase 3 study (LIBERTY AD CHRONOS), adults with moderate-to-severe atopic derma

178 ying the classical nova eruption of 11 March AD 1437, and independently confirm its age by proper-mot

179 ient-reported moderate and severe AD vs mild AD were associated with significantly higher oSCORAD, SC

180 tic medication use, while patients with mild AD only had increased risk of anxiolytic medication use.

181 efficacy of verubecestat in mild-to-moderate AD raises important questions about the timing of interv

182 16 in the United States for mild-to-moderate AD, with other PDE4 inhibitors, an agonist of the aryl h

183 -TNF-alpha therapy or RA itself can modulate AD pathology, although the underlying mechanism is uncle

184 l for both clinical diagnosis and monitoring AD disease progression.

185 he bilingual, compared with the monolingual, AD patients.

186 significantly more cases categorised as non-AD dementia post-API (from 11 to 23).

187 oys (36.1%) and 350 girls (63.9%) in the non-AD group (data on gender identification were missing for

188 tes were observed in lesional vs nonlesional AD, TCR repertoire diversity was similar in lesional and

189 h DHA supplementation in predementia but not AD dementia suggests that early omega-3 supplementation

190 althy controls and to investigate aspects of AD related to ADHD symptoms.

191 relationships between age, CSF biomarkers of AD pathology, and quantitative magnetic resonance imagin

192 nisms by which microglia alter the course of AD neuropathology remain poorly understood.

193 tion in promising tasks for the detection of AD.

194 ght protect against the later development of AD.

195 e to Abeta deposition and the development of AD.

196 Although definitions and diagnosis of AD have largely been agreed upon, allergists and dermato

197 isms involved in the ameliorating effects of AD symptoms observed in AD/TTR(+/-) animal models after

198 mer disease (AD) pathology and expression of AD symptoms is poorly understood.

199 M344 increases the expression of AD-relevant genes: BDNF, alpha-secretase (ADAM10), MINT2

200 minant forms of Abeta in aqueous extracts of AD brain are high molecular weight (HMW) and relatively

201 A hallmark of AD is disruption of the critical barrier function of upp

202 To identify adults with a history of AD, we used a question regarding physician-diagnosed AD

203 cks, in adults with and without a history of AD.

204 mising approach to decrease the incidence of AD.

205 nd divergent approaches to the management of AD.

206 ola oil on the phenotype of a mouse model of AD that develops both plaques and tangles (3xTg).

207 act system, is increased in a mouse model of AD, and this cleavage is temporally correlated with the

208 oved cognition and in an aggressive model of AD.

209 agonist bexarotene in an aggressive model of AD.

210 of BACE1 S-palmitoylation in mouse models of AD amyloidosis.

211 d synapses in in vivo and in vitro models of AD and frontotemporal dementia (FTD).

212 Results in animal and cellular models of AD and in patients with sporadic late-onset AD suggest t

213 and blood, more complex biomarker models of AD are needed.

214 In cell models of AD, however, the concentration of unprocessed C99 increa

215 tation in APOE4 carriers before the onset of AD dementia can be a promising approach to decrease the

216 ay reduce the risk for or delay the onset of AD symptoms in APOE4 carriers.

217 in causal agent associated with the onset of AD.

218 he long latency and incomplete penetrance of AD dementia with respect to Abeta pathology, we hypothes

219 rapeutic target in the preclinical phases of AD.

220 The presence of AD was examined in 2 birth cohort studies including 9894

221 The prevalence of AD in longitudinal birth cohort studies is similar in ch

222 ther there is a decline in the prevalence of AD in population-based cohorts of patients followed long

223 Promotion of AD-related signaling pathways through this mechanism may

224 r the effective treatment of a wide range of AD-like pathophysiological and cognitive impairments.

225 ethylation alterations influence the risk of AD-ND codependence or the other way around.

226 The RP of AD was 5% (RPtrend, 1.05; 95% CI, 1.03-1.07) higher for

227 ingle correlations with severity (Scoring of AD, or SCORAD) are detected not only in lesional but als

228 rse of IVIG administered in the MCI stage of AD reduces brain atrophy, prevents cognitive decline in

229 s of 20 OMPs during the methanogenic step of AD with a focus on the role of acetate kinase (AK), whic

230 re identified, representing subphenotypes of AD, with remarkable consistency between the 2 cohorts.

231 esveratrol in the prophylaxis and therapy of AD.

232 get disease-modifying drugs for treatment of AD and/or similar neuropathologies.

233 pment of lead compounds for the treatment of AD.

234 We demonstrate the utility of AD-LIBS with synthetic data.

235 Only AD (FLG/WT) HEEs exhibited significantly increased level

236 and study of inherited forms of early-onset AD and genetic risk factors that provide insights about

237 AD and in patients with sporadic late-onset AD suggest that impaired mitophagy contributes to synapt

238 Postpartum AD was defined as use of antidepressants and/or hospital

239 g the nature of myelin damage in preclinical AD may be informative on the disease's course and lead t

240 nectivity phase in the course of preclinical AD.SIGNIFICANCE STATEMENT This article offers a first lo

241 ognitive decline associated with preclinical AD.SIGNIFICANCE STATEMENT Understanding how risk factors

242 One predominately AD subtype (with a large proportion of SQCC) shared mole

243 oftener in early life may be able to prevent AD development.

244 ould help the clinical diagnosis of probable AD.

245 istic biomarkers to distinguish the probable AD group from the healthy group.

246 mparison with AD subjects without psychosis, AD+P subjects have more rapid cognitive decline and poor

247 oL (Quality of Life Alzheimer's Disease [QoL-AD]) for the person with dementia and general health sta

248 ered that A673V mutation, the only recessive AD-associated APP mutation, shifted the preferential bet

249 ontrols identified eight previously reported AD risk loci and 14 novel loci associated with age at on

250 Patient-reported moderate and severe AD vs mild AD were associated with significantly higher

251 n the health registry study, moderate-severe AD patients had increased risk of antidepressant and anx

252 as significantly related to both more severe AD-associated neurodegeneration (lower ADSCT scores) and

253 era from 20 subjects with moderate to severe AD, 10 subjects with CD, 12 subjects with moderate to se

254 ildren and 34 adults with moderate-to-severe AD (mean SCORAD score, 55 and 65, respectively) and age-

255 roteomic assay to analyze moderate-to-severe AD (n = 59) compared to psoriasis (n = 22) and healthy c

256 experience adequate response after a single AD trial, and this variability remains poorly understood

257 se in alleviating cognitive symptoms in some AD patients.

258 ants has discovered coding mutations in some AD-associated genes, a lot of risk variants lie in nonco

259 at risk of developing AD and/or early stage AD for which current therapies may be more beneficial.

260 7C3-S243 blocked neurodegeneration in TgF344-AD rats, without altering amyloid deposition or indicato

261 s the first line of evidence to suggest that AD-associated neurodegeneration links to altered PNS reg

262 hat additionally to its local actions in the AD brain, TNF-alpha can also indirectly modulate amyloid

263 89 boys (34.2%) and 363 girls (65.8%) in the AD group and 198 boys (36.1%) and 350 girls (63.9%) in t

264 sible for the Hcy-dependent worsening of the AD phenotype in a relevant mouse model of the disease.

265 expression levels influence the onset of the AD-like phenotype in mouse models.

266 d mortality after developing dementia or the AD subtype of dementia, separately, using adjusted Cox p

267 In conclusion, LHPP locus is associated to AD-RSB interaction; and with brain circuitries previousl

268 od, we reconstructed NAO-like phases back to AD 1650.

269 of the south-central Andes) during 400 BC to AD 1000 (part of the regional Formative Period), with a

270 ive decline in LMCI and delays conversion to AD dementia for at least 1 year; however, this effect of

271 ND Building on prior work linking the HLA to AD, we used a robust imputation method on two separate c

272 ature review on RA incidence and its link to AD was carried out according to the PRISMA guidelines.

273 E score only, the 3-year progression risk to AD dementia ranged from 26% (95% CI, 19%-34%) in younger

274 sm may contribute to female vulnerability to AD.

275 ventually for designing new molecules toward AD therapeutic drugs.

276 Effective strategies to prevent and treat AD remain elusive despite major efforts to understand it

277 een Abeta and Drp1 is reduced in DDQ-treated AD neurons.

278 and Drp1 levels were reduced in DDQ-treated AD neurons.

279 represent an effective approach to treating AD.

280 e mononucleotide and (tz) ATP to yield N(tz) AD(+) , which can be enzymatically phosphorylated by NAD

281 N(tz)AD(+) and N(tz)ADH serve as substrates for NADase, which

282 A drop in fluorescence is seen as N(tz)AD(+) is converted to N(tz)ADH, reflecting a complementa

283 Clinical end points were AD dementia and any type of dementia after 1 and 3 years

284 lot analysis (15 young, 24 aged, and 21 with AD).

285 with AD progression, and is associated with AD pathologic findings at autopsy.

286 sychosocial characteristics of children with AD, ADHD, comorbid AD/ADHD and age-matched healthy contr

287 In comparison with AD subjects without psychosis, AD+P subjects have more r

288 carbon storage and water conservation, with AD second.

289 n=20), MCI with DLB profile (n=38), MCI with AD profile (n=20) and healthy control subjects (n=20).

290 ntramuscular, vaccination, participants with AD with S aureus colonization experienced (1) lower sero

291 nza H1N1 than noncolonized participants with AD.

292 levels were seen in pediatric patients with AD (P < .0001).

293 with MCI (mean, 42.8 ng/L) and patients with AD dementia (mean, 51.0 ng/L) compared with controls (me

294 However, not all patients with AD have FLG mutations.

295 erved cognitive performance in patients with AD pathology.

296 d high diagnostic accuracy for patients with AD with dementia vs controls (area under the receiver op

297 cognitive impairment, and 180 patients with AD with dementia, plasma NFL correlated with CSF NFL (Sp

298 precedes cognitive deficits in patients with AD.

299 ical Alzheimer disease (AD), progresses with AD progression, and is associated with AD pathologic fin

300 NL levels have been associated recently with AD.

301 will help to determine subphenotypes within AD that predict prognosis and treatment responses.