ライフサイエンスコーパス: age at onset

1 d after conditioning on disease location and age at onset.

2 ual's polygenic risk score and their disease age at onset.

3 ygenic score for PD risk alleles and disease age at onset.

4 manifestations including a wide spectrum of age at onset.

5 ession in PPMS is variable and influenced by age at onset.

6 eneous, with variable tissue involvement and age at onset.

7 compared clinical characteristics, including age at onset.

8 the SPG4 mutations was found to predict the age at onset.

9 41-0.75]) after adjustment for age, sex, and age at onset.

10 her expression was associated with a delayed age at onset.

11 D subtypes only when data were stratified by age at onset.

12 composed of two subgroups, differentiated by age at onset.

13 N, with no effects of duration of illness or age at onset.

14 terminants of the progression of disease and age at onset.

15 D could be identified in cases subdivided by age at onset.

16 patients with strong family history or early age at onset.

17 risk loci and 14 novel loci associated with age at onset.

18 sis was derived using DSM-5 criteria, except age at onset.

19 teria for young adult ADHD (YA-ADHD), except age at onset.

20 We conducted a genome-wide study for age-at-onset.

21 hort duration of follow-up (p<0.0001), lower age at onset (-0.02 [SE 0.01] per additional year; p=0.0

22 nteen patients (median [interquartile range] age at onset, 1.5 [9.8] years) with YARS2-related mitoch

23 verage 5.6 years younger than their expected age at onset; 20 healthy control subjects were also stud

24 The 10 cases expand both the known age at onset (28 to 92 years, median 68) and clinical fe

25 ly 3 with a presumed recessive transmission (age at onset, 38 years; mean visual acuity, 20/50).

26 and driven by inclusion of SNCA p.A53T (mean age at onset, 45.9 years; 95% CI, 43-49 years).

27 Of 250 patients (mean [SD] age at onset, 49.7 [21.2] years; 56% female), 38 (15.2%)

28 han 65 years) into early-onset (n = 21, mean age-at-onset 55.2 +/- 5.9 years) and late-onset (n = 18,

29 Four GRN mutation carriers (age at onset, 56-65 years) presenting with severe WML we

30 re comparable to Tunisian Arab Berbers (mean age at onset, 57.1 years; 95% CI, 45.5-68.7 years) (P =

31 hkenazi Jewish LRRK2 p.G2019S carriers (mean age at onset, 57.9 years; 95% CI, 54-63 years) were comp

32 without routine cardiac assessment (average age at onset, 58.8 years).

33 e [60.8%] and 1667 female [39.2%]; mean [SD] age at onset, 59 [12] years), the following 2 novel loci

34 TTR were assessed; 37 were symptomatic; mean age at onset=62 years, range=38-75 years; 75.7% male.

35 (P = .58), whereas Norwegian carriers (mean age at onset, 63 years; 95% CI, 51.4-74.6 years) were si

36 period, a total of 2702 patients (mean [SD] age at onset, 65.7 [11.1] years; 1246 [46.1%] female and

37 on with genotype but an association with the age at onset; 7 new SPG4 mutations were identified; and

38 s as they also developed AD dementia (median age at onset, 76.0 years).

39 heterozygous for A673T, including 1 AD case (age at onset, 89 years) and 2 controls (age at last exam

40 An earlier age at onset (AAO) has been associated with greater gene

41 Age at onset (AAO) in multiple sclerosis (MS) is an impo

42 rstanding how midlife risk factors influence age at onset (AAO) of Alzheimer's disease (AD) may provi

43 ion testing to identify variants that modify age at onset (AAO) of Alzheimer's disease.

44 Age at onset (AAO) of bipolar disorders (BD) could be in

45 zheimer disease (LOAD) and to differences in age at onset (AAO), it is important to know whether othe

46 d psychiatric symptoms, imaging results, and age at onset (AAO).

47 In addition to the disease risk, age-at-onset (AAO) of AD has also strong genetic compone

48 itional Mendelian gene variants have younger ages at onset (AAO).

49 evolving retinal dystrophies, assessment of age at onset, accurate clinical diagnosis, and genetic t

50 st that a common genetic mechanism modulates age at onset across polyglutamine diseases and could ext

51 2 repeat expansion by means of a decrease in age at onset across successive generations.

52 ns were identified in exons 1 and 2 in early-age-at-onset advanced POAG cases.

53 Male sex (HR=1.41; p<0.001), older age at onset (age </=20 and 21-30 vs >30 HR=0.52 (p<0.00

54 meostasis modulator 1), a gene modulating AD age at onset and Abeta metabolism.

55 assessed the association of repeat size with age at onset and age at collection using a Spearman's te

56 AG repeat size is the primary determinant of age at onset and age at death in HD.

57 106B may act as a genetic modifier affecting age at onset and age at death in the Mendelian subgoup o

58 survival in this cohort was associated with age at onset and age at diagnosis only.

59 actinic dermatitis presents with an earlier age at onset and an inverted male to female ratio in pat

60 reflected by a quadratic association between age at onset and CAG size in spinocerebellar ataxia type

61 Positive associations were stratified by age at onset and cancer family history.

62 ADAD phenotypes are heterogeneous, with both age at onset and clinical features being influenced by m

63 ele of rs3764650 in ABCA7 is associated with age at onset and disease duration, and the minor allele

64 We assessed the effect of TREM2 genotype on age at onset and disease duration.

65 study (GWAS) in HD found association between age at onset and genetic variants in DNA repair pathways

66 MDD patients with early age at onset and higher symptom severity have an increas

67 g the patients, there was variability in the age at onset and in the specific pattern of photorecepto

68 ilon4 risk allele associates with an earlier age at onset and increased amyloid-beta deposition, wher

69 good agreement with the physician-confirmed age at onset and last disease activity; the mean differe

70 The age at onset and natural progression of retinal disease

71 nd relationship status) and psychiatric (ie, age at onset and number of previous episodes of depressi

72 un damage and round cell melanoma with early age at onset and phototype 1 in the context of multiple

73 Both age at onset and progression of the disease showed clini

74 ies, because rare variants contribute to the age at onset and progression of the disease.

75 minant Alzheimer's disease has a predictable age at onset and provides an opportunity to determine th

76 ogressive cerebellar ataxia, with a variable age at onset and rate of progression between different b

77 l features of disease such as female gender, age at onset and severity.

78 evidence regarding the prognostic effect of age at onset and stridor.

79 A higher HLAGB was associated with younger age at onset and the atrophy of subcortical gray matter

80 ith SARA were explained by disease duration, age at onset and the shorter abnormal repeat in the FXN

81 rabismus subtypes, indicating differences in age at onset and thereby implying differences in the und

82 me since most recent episode controlling for age at onset and time since onset.

83 5), while no correlations were found between age-at-onset and [(11)C]-labelled Pittsburgh compound-B

84 phenotypes (e.g., binary, quantitative, and age at onset), and it allows arbitrary covariates (e.g.,

85 rtex, is related to PMDD severity, symptoms, age at onset, and disease burden.

86 Multivariable analysis adjusted by sex, age at onset, and disease duration attributed to GBA car

87 and lifetime psychiatric disorders, disorder age at onset, and disorder severity in a nationally repr

88 location, disease behavior, disease course, age at onset, and extraintestinal manifestations).

89 on, age of patient or unaffected individual, age at onset, and first motor symptom of patient.

90 related to lifetime cannabis use (ever used, age at onset, and frequency of use) using linear regress

91 have found an increased prevalence, younger age at onset, and more severe course of glaucoma in peop

92 ombination of anatomical pattern of atrophy, age at onset, and neuropsychiatric characteristics of th

93 isk, and associations with symptom severity, age at onset, and parental psychiatric history.

94 pressive agents), whereas clinical features, age at onset, and pathologic findings were similar in st

95 The high heritability, early age at onset, and reproductive disadvantages of autism s

96 hermore, pathologic mechanisms may vary with age at onset, and understanding these processes may lead

97 ve generations), although the differences in age at onset are not entirely accounted for by repeat le

98 ermined using general linear models with the age at onset as the dependent variable.

99 estimated using the Kaplan-Meier method with age at onset as the time variable; asymptomatic carriers

100 Among the 111 individuals with age at onset available (66 men and 45 women; mean [SD] a

101 Age at onset, baseline MMSE, years of education, motor e

102 to -0.14; P = .02) and in those with a later age at onset (beta, -0.11; 95% CI, -0.14 to -0.08; P < .

103 ost-enlistment (chi(7)(2) = 123.8, P < .001) ages at onset both significantly predicted severe role i

104 AG repeat tracts are associated with earlier ages at onset, but this does not account for all of the

105 ical features of early relapse frequency and age at onset can be used to select groups at higher risk

106 ncidence in most Asian countries, an earlier age at onset compared with the West, a relative increase

107 Age-at-onset correlated positively with glucose metaboli

108 sex, duration of illness (current age minus age at onset), course (single episode or recurrent depre

109 were stratified using increasing/decreasing age-at-onset cutoffs; significant single nucleotide poly

110 In the 8451 patients for whom age at onset data were available, deletions at 22q11.2 w

111 Age at onset differed by mutation, with a younger onset

112 ying a C9orf72 repeat expansion by analyzing age at onset, disease duration, and age at death in succ

113 The generational effect on age at onset, disease duration, and age at death was est

114 Generational effect on age at onset, disease duration, and age at death.

115 Data concerning demographics, age at onset, disease duration, and clinical and patholo

116 stage, but not Thal amyloid phase predicted age at onset, disease duration, and final Mini-Mental St

117 Clinical presentation, age at onset, disease duration, and rate of cognitive de

118 gnetic resonance imaging outcomes, including age at onset, disease severity, conversion time from cli

119 with the susceptibility probability and the age-at-onset distribution of susceptible individuals for

120 Age at onset does not influence amyloid deposition or ne

121 The cases were also evaluated for age at onset effects (</= or >8 years of age).

122 loci and age at onset is the first report of age at onset effects in allergic rhinitis.

123 Two loci showed significant age at onset effects, but the effect of asthma on the as

124 Subgroup meta-analysis assessing age-at-onset effects identified reduced GMV in the left

125 and substance use disorders have an earlier age at onset, greater symptom severity, more comorbidity

126 entation did not correlate with outcome, but age at onset >/= 4 months was associated with attenuated

127 t onset </=16 years) and late-onset smokers (age at onset >16 years), and a logistic regression of he

128 at onset <60 years old and 36 patients with age at onset >70 years old.

129 Age at onset has been used as a quantitative phenotype i

130 The clinical features (age at onset, high prevalence in women, frequency and se

131 Demographic characteristics, age at onset, history of depression in first-degree rela

132 y disease in several ways, including younger age at onset, history of infantile liver involvement, an

133 age-related macular degeneration and earlier age at onset; however, its associated phenotype has not

134 rithm of odds] score, 3.69), and the GWAS of age at onset identified variants on 1p13.1, 2q13, 4q25,

135 partum episodes were associated with younger age at onset, illness during pregnancy, bipolar disorder

136 and SORBS2 may serve as genetic modifiers of age at onset in both EOAD and LOAD.

137 -related frontotemporal dementia and affects age at onset in GRN mutation carriers.

138 w that DNA repair genes significantly modify age at onset in HD and SCAs, suggesting a common pathoge

139 ociation study detected genetic modifiers of age at onset in Huntington's disease.

140 ral gyrus was negatively correlated with the age at onset in IGE patients.

141 Given prior evidence of heterogeneity by age at onset in MDD, we tested whether genome-wide signi

142 familial Alzheimer disease (AD) by examining age at onset in PSEN1 mutation carrier families, and fur

143 ed at-risk relatives confirmed a decrease in age at onset in successive generations (P < .001).

144 prior evidence for strong genetic effect on age-at-onset in familial PD.

145 Neither LHFPL2 nor TPM1 was associated with age-at-onset in non-familial PD.

146 (CPD >20) and light smokers (CPD </=10) with age-at-onset information, reducing the sample size to 33

147 is increased genetic burden by performing an age-at-onset informed GWAS meta-analysis, including a la

148 We used a three-stage age-at-onset informed GWAS to identify novel genetic var

149 Importantly, we also show that age at onset is further modified by the level of somatic

150 pinocerebellar Ataxias, to determine whether age at onset is influenced by the size of the normal all

151 As the variability in age at onset is not completely explained by the effects

152 the SSTR1-MIPOL1 and TSLP-SLC25A46 loci and age at onset is the first report of age at onset effects

153 the expansion is negatively correlated with age at onset, it accounts for only 50-70% of its variabi

154 udy was stratified into early-onset smokers (age at onset </=16 years) and late-onset smokers (age at

155 iance and 1.1% (p = 1.30e(-05)) for MDD with age at onset <18 years.

156 utations with particularly early onset (mean age at onset <40 years) involving PSEN1's first hydrophi

157 D pathophysiologic process: 24 patients with age at onset <60 years old and 36 patients with age at o

158 non-Hispanic white (NHW) patients with EOAD (age at onset <65 years) and 19 Caribbean Hispanic famili

159 tients with early-onset Alzheimer's disease (age at onset <65 years), 12 patients with logopenic vari

160 three clinical AD variants: early-onset AD (age at onset, <65 y; memory and executive deficits), log

161 1.2 were associated with Parkinson's disease age at onset (Mann-Whitney U test p=0.001).

162 y determinant of outcome, although the later age at onset may make it difficult to discern if aortic

163 Intermittent explosive disorder had an early age at onset (mean age, 12.0 years) and was highly persi

164 We reviewed patient medical records for age at onset, medical history, initial symptoms, best-co

165 A medical record review of 55 patients for age at onset, medical history, initial symptoms, best-co

166 nal success in identifying risk loci but not age-at-onset modifiers.

167 th the strongest risks associated with young age at onset, multiple affected relatives, and in first-

168 g all significant risk factors, were younger age at onset (odds ratio=0.94, 95% CI=0.90-0.99), poorer

169 nset rod-cone dystrophy, with a mean (range) age at onset of 12.1 (7-17) years.

170 females) had new-onset MDD, with a mean (SD) age at onset of 14.4 (2.0) years (range, 10-18 years).

171 nset rod-cone dystrophy, with a mean (range) age at onset of 29.7 (20-40) years, and 6 had an earlier

172 Mean age at onset of 30.7 years did not differ significantly

173 9 to 83 years at diagnosis, with a mean (SD) age at onset of 42.6 (2.4) years and duration of disease

174 rt (32.6% [16 of 49] female) had a mean (SD) age at onset of 50.1 (15.7) years.

175 rt (49.5% [46 of 93] female) had a mean (SD) age at onset of 61.8 (10.0) years.

176 re women, 203 were men, they had a mean (SD) age at onset of 64.8 (10.2) years, and 37 of them carrie

177 Older age at onset of allergies was slightly more protective t

178 Of these 5 patients, 4 were men (80%); mean age at onset of ALSP was 29 years (range, 15-44 years).

179 al of 76.6% of cases reported pre-enlistment age at onset of at least one 30-day disorder (49.6% inte

180 erted to multiple system atrophy had younger age at onset of autonomic failure, severe bladder/bowel

181 na and high-income countries include younger age at onset of breast cancer; the unique one-child poli

182 Mean age at onset of clinical symptoms was 20.3 years in pati

183 Mean age at onset of CNV was 54.4 +/- 14 years.

184 ciated epilepsy at our center included early age at onset of cognitive decline, early incidence of se

185 The G allele of rs2238126 confers earlier age at onset of colorectal cancer (P=1.98 x 10(-6)) and

186 , adjusted for age, sex, diagnostic subtype, age at onset of dementia, and significant vascular risk

187 Age at onset of disease decreases with increasing polygl

188 damage-response and repair pathways and the age at onset of disease.

189 ding dystonia aetiology, dystonia phenotype, age at onset of dystonia, and duration of dystonia prior

190 , PDLIM3, and SORBS2 as genetic modifiers of age at onset of EOAD and LOAD and provided modest suppor

191 terval before antiepileptic drug withdrawal, age at onset of epilepsy, history of febrile seizures, n

192 ition and age at onset of ESRD, with younger age at onset of ESRD associated with mutations at the 5'

193 The median age at onset of ESRD was 55 years for carriers of a trun

194 The median age at onset of ESRD was 58 years for PKD1 carriers and

195 tients with regard to predialysis eGFR, sex, age at onset of ESRD, or duration of diabetes.

196 g relationship between mutation position and age at onset of ESRD, with younger age at onset of ESRD

197 Median age at onset of eye disease was 60 months and duration o

198 netic modifiers that may delay or accelerate age at onset of familial Alzheimer disease (AD) by exami

199 The median age at onset of HPFS was 5 years; median age at presenta

200 he expanded CAG tract in HTT correlates with age at onset of Huntington's disease and other trinucleo

201 sine-adenine-guanine (CAG) repeat length and age at onset of Huntington's disease is well known, impr

202 mutated gene and type of mutation influence age at onset of Lynch syndrome-associated cancers.

203 l, multivariate analyses that controlled for age at onset of major depressive disorder, the number of

204 eta-analyze studies evaluating the effect of age at onset of menopause and duration since onset of me

205 e-control, or cross-sectional) that assessed age at onset of menopause and/or time since onset of men

206 rol, or cross-sectional studies; reported on age at onset of menopause and/or time since onset of men

207 hat better course was associated with higher age at onset of mood symptoms, less lifetime family hist

208 G allele size and negatively correlated with age at onset of motor symptoms.

209 imary driver of the processes that determine age at onset of motor symptoms.

210 In total, 275 patients with a known age at onset of neovascular AMD and a genetic risk analy

211 aphic, behavioral, and ocular factors on the age at onset of neovascular AMD.

212 and environmental risk factors influence the age at onset of neovascular AMD.

213 Median age at onset of neurologic symptoms was 58 (range, 27-83

214 kground have been shown to contribute to the age at onset of neurological symptoms.

215 Age at diagnosis; age at onset of night blindness, visual field loss, visu

216 Younger baseline age, younger age at onset of ocular VHL disease, involvement of the f

217 Age at onset of Parkinson's disease was lower in patient

218 Carriers had an earlier age at onset of PD (P < .001) and were younger (P = .004

219 Age at onset of persistent wheeze in the first 3 years o

220 Age at onset of progressive biomarker changes that disti

221 calculated the weighted mean difference for age at onset of psychosis and age at initiation of smoki

222 h increased risk of psychosis and an earlier age at onset of psychotic illness.

223 , that smoking is associated with an earlier age at onset of psychotic illness.

224 viously reported association between younger age at onset of RA and a RANKL promoter SNP that conferr

225 genetic and familial-environmental effects, age at onset of regular smoking predicted level of nicot

226 in pairs who differed by at least 2 years in age at onset of regular smoking.

227 d Substance Use Disorders for discordance in age at onset of regular smoking.

228 The age at onset of retinal dystrophy was variable.

229 No significant effects of age at onset of schizophrenia or medication dosage were

230 Because of this shift, the age at onset of severe obstruction has changed from the

231 Mean age at onset of symptoms was 42.7 years.

232 carriers and noncarriers of rare variants in age at onset of symptoms, the family history of AMD, com

233 The median age at onset of the cases was significantly younger than

234 The mean age at onset of the disease was 2.6 +/- 2.4 years (range

235 The mean age at onset of the hallucinations was 56 years, ranging

236 ground strongly influenced the magnitude and age at onset of these effects.

237 ation was apparent with offspring's smoking, age at onset of tobacco use, or changes in use between 2

238 The age at onset of treatment was 2-28 months.

239 Homozygosity was associated with earlier age at onset of tremor (P < 0.0001), more severe postura

240 nvironmental factors (trauma exposure, early age at onset of use, and environmental hardship) to prod

241 statistical methods tailored to address the age at onset of various forms of G1D, associated manifes

242 in risk, incidence, prevalence, severity and age-at-onset of many diseases.

243 nes are thought to have a stronger effect on age-at-onset of PD than on risk, yet there has been a ph

244 easures such as COX-deficient fibre density, age-at-onset of symptoms and progression of disease burd

245 progression of the syndrome, we studied the ages at onset of 5 cardiometabolic diseases: abdominal o

246 Median (interquartile range) ages at onset of catecholaminergic polymorphic VT sympto

247 ophic lateral sclerosis have highly variable ages at onset of disease, suggesting the presence of mod

248 tecting genetic interactions associated with age-at-onset outcomes.

249 The groups had different ages at onset, overall survival, and associations with g

250 ng of milestones were strongly influenced by age at onset (P < 0.0001) and by total disease duration

251 0001, OR 3.50 [95% CI 2.63- 4.63]) and early age at onset (P < 0.0001).

252 gnificantly higher than in those with a late age at onset (p = 0.00014).

253 oid-beta score (P=0.017) along with an older age at onset (P=0.001) were associated with a shorter ti

254 ample) that is significantly correlated with age at onset (p=2 x 10(-89)).

255 n [SD] age, 57.2 [9.1] years), the mean (SD) age at onset per generation (from earliest-born to lates

256 pregnancy, in descending order, were younger age at onset, previous postpartum episodes, fewer years

257 ents with FTD, repeat length correlated with age at onset (r=0.63; p=0.003) and age at sample collect

258 as the cause of different types of NCL, with ages at onset ranging from around birth to adult, althou

259 ith rLETM or rLETM-onset NMO were similar in age at onset, sex ratio, attack severity, relapse rate,

260 under an additive model with adjustment for age at onset, sex, and the first 4 principal components

261 Meta-analysis was performed within each age-at-onset stratum.

262 ich repeat length does not contribute toward age at onset, suggesting pathogenesis is not constrained

263 Even when adjusted for age at onset, symptom duration, and other demographic va

264 developed PD, patients with GD had a younger age at onset than GBA heterozygotes (mean, 54.2 vs 65.2

265 rrelated with each other (r=0.674), and with age at onset (TRACK-HD, r=0.315; REGISTRY, r=0.234).

266 ransition experience can be distinguished by age at onset, variability of the menstrual cycle, and du

267 y, p<0.0001); within the PSEN1 group, 72% of age at onset variance was explained by the specific muta

268 The age at onset varied widely, from 2 to 54 years.

269 Age at onset, visual acuity survival time, visual acuity

270 Age at onset was 17-50 years in 99%, the same age range

271 The mean age at onset was 33 years (range, 17-43 years), and the

272 Mean age at onset was 34 years; all cases were compound heter

273 The mean age at onset was 34.1 years.

274 Compared with the reference group, the age at onset was 5.2 (95% CI, 2.8-7.7) years earlier for

275 e included; 1310 (66%) were women and median age at onset was 55 years (IQR 43-66).

276 The mean age at onset was 55 years (range, 45-72 years).

277 The median age at onset was 56.0 years and was higher among women t

278 The mean age at onset was 7.2 years (range, 1-10).

279 tients with PD, 275 were men, and the median age at onset was 73 years (interquartile range, 64-80 ye

280 h parkinsonism, 501 were men, and the median age at onset was 74 years (interquartile range, 66-81 ye

281 The mean age at onset was 9 years lower in index patients with 2

282 In particular, age at onset was a highly significant predictor but only

283 ividuals with spinocerebellar ataxia type 1, age at onset was also influenced by other (CAG)n-contain

284 Age at onset was assessed retrospectively.

285 Older age at onset was independently associated with a poorer

286 Between July 1, 1987, and Oct 31, 2015, age at onset was recorded for 213 patients (168 with PSE

287 enic score in patients with an early disease age at onset was significantly higher than in those with

288 ies accounted for 12.4%, and their mean (SD) age at onset was similar to those of the HD-HTT group (4

289 Principal components analysis showed that age at onset was the major classifier of samples from pa

290 The age at onset was variable and ranged between 9 and 58 ye

291 The average age-at-onset was 17.9 years (range 5 months to 35 years)

292 dy mass index, and to study the influence of age at onset, we pooled data from 10 case-control studie

293 The effects of age at onset were attenuated in youths with lower socioe

294 The mean differences in the age at onset were determined using general linear models

295 found the most significant association with age at onset when grouping all polyglutamine diseases (H

296 ifference between age at assessment and mean age at onset within the family.

297 conomic disparities in disease incidence and age at onset within the same nation point to a potential

298 After pediatric onset MS (POMS) diagnosis, age at onset younger than 15 years and DMD exposure decr

299 re particularly enriched among cases with an age at onset younger than 18 (OR = 6.3 [1.7,22.6], p = 0

300 ode of diverticulitis is rare (<5%) and that age at onset younger than 50 years and 2 or more recurre