ライフサイエンスコーパス: biological aging

1 mmunological contribution to the accelerated biological aging.

2 d its treatments may also be associated with biological aging.

3 rectly through LTL, an integrative marker of biological aging.

4 eration (EAA), which may reflect accelerated biological aging.

5 racteristics are associated with accelerated biological aging.

6 accumulate with each pregnancy, accelerating biological aging.

7 Exposure to adversity can accelerate biological aging.

8 ion in childhood had the highest accelerated biological aging.

9 hy diets have been inversely associated with biological aging.

10 ity is an important correlate of accelerated biological aging.

11 physical illnesses suggestive of accelerated biological aging.

12 n rate in a manner comparable to cellular or biological aging.

13 se benefits operate through a slowed pace of biological aging.

14 casting obesity as a disease of accelerated biological aging.

15 premature mortality, suggesting accelerated biological aging.

16 ovascular disease (CVD) risk and accelerated biological aging.

17 nic immune stimulation and may contribute to biological aging.

18 schizophrenia is accompanied by accelerated biological aging.

19 Several chronic diseases accelerate biological aging.

20 essing the effects of smoking on the rate of biological aging.

21 appear to be highly conserved mechanisms of biological aging.

22 new insight into the factors that influence biological aging.

23 apoptosis constituting an integral aspect of biological aging.

24 ty and may be a marker of general health and biological aging.

25 ns, common lifestyle and health factors, and biological aging.

26 ng epigenetic age acceleration - a marker of biological aging.

27 cause there is no widely accepted measure of biological aging.

28 the progressive and unidirectional nature of biological aging.

29 estigate the role of adolescent lifestyle in biological aging.

30 ecular changes relevant to chronological and biological aging.

31 he age of smoking initiation and accelerated biological aging.

32 tered epigenome and telomere maintenance and biological aging.

33 suggest that GLTD is an integral element of biological aging.

34 gainst dementia because it slows the pace of biological aging.

35 an be lost because of noise over exposure or biological aging.

36 Telomere length is a molecular marker of biological aging.

37 Telomere length is considered a biomarker of biological aging.

38 onsequences contributing to disease risk and biological aging.

39 n age-dependent functional decline, known as biological aging.

40 division, are considered reliable markers of biological aging.

41 psychoactive medication do further impact on biological aging.

42 linked to commonly-used clinical measures of biological aging.

43 may be a key factor in HIV-related premature biological aging.

44 Telomere length may be a marker of biological aging.

45 ium surfaces, indicating a titanium-specific biological aging.

46 nditions of oxidative stress observed during biological aging.

47 Reduced telomere length may be a marker of biological aging.

48 ementia and mortality and may be a marker of biological aging.

49 ybrid rats, a well accepted animal model for biological aging.

50 on during development, oxidative stress, and biological aging.

51 ks support the applicability of the model to biological aging.

52 gle-time-point measure of a person's pace of biological aging.

53 els under conditions of oxidative stress and biological aging.

54 chemical or photochemical modifications, not biological aging.

55 help us to better comprehend the process of biological aging.

56 somatic maintenance and repair, accelerating biological aging.

57 apies designed to prevent disease by slowing biological aging.

58 age, with positive values suggesting faster biological aging.

59 and neuroendocrine dysregulation as well as biological aging.

60 affect health and mortality, but its link to biological aging-a precursor of the morbidity and mortal

61 hronic environmental stressors to accelerate biological aging across multiple organ systems.

62 and tobacco use were associated with faster biological aging across several clocks; associations wit

63 aturation and both embryonic development and biological aging across species.

64 re that is sensitive to variation in pace of biological aging among individuals born the same year.

65 l deficit accumulation represents underlying biological aging among survivors of cancer.

66 This suggests mechanisms of accelerated biological aging among the depressed, which can be indic

67 of vascular disease is linked to accelerated biological aging and a combination of genetic, lifestyle

68 ensure robust hematopoietic function during biological aging and after exposure to acute stress.

69 ohort study examines the association between biological aging and all-cause and cardiovascular diseas

70 , durable therapeutics that act against both biological aging and Alzheimer's disease is an unmet cli

71 Telomere shortening, which is a biomarker of biological aging and chronic disease, may be associated

72 nAGE at age 45 years, as well as the pace of biological aging and cognitive decline in longitudinal d

73 to determine the heterogeneous trajectory of biological aging and disease manifestation.

74 tions within tissues could be informative of biological aging and disease risk.

75 early-life tobacco exposure with accelerated biological aging and further assessed the joint effects

76 udies, with support from animal research, on biological aging and illnesses.

77 ing and burden of these infections influence biological aging and immune function across the life cou

78 iency and discuss the actions of GH/IGF-1 on biological aging and lifespan.

79 EAA measurements known to be associated with biological aging and long-term health: intrinsic EAA (IE

80 Telomere length reflects biological aging and may be influenced by environmental

81 urther, anxiety and depression are linked to biological aging and may contribute to the poor long-ter

82 ondition that is associated with accelerated biological aging and multiple end-organ morbidities.

83 educational attainment may slow the pace of biological aging and promote longevity.

84 so SA, may be associated with an accelerated biological aging and provide putative biological mechani

85 Our results suggest that both biological aging and reduced regenerative capacity contr

86 human cohorts highlights the role of RTEs in biological aging and suggests possible mechanisms and ce

87 th the hypothesis that pregnancy accelerates biological aging and that these effects can be detected

88 study investigates the relationships between biological aging and various dietary factors within the

89 ights into molecular processes that underlie biological aging and, perhaps more importantly, potentia

90 ios were 1.71-2.32 per standard deviation of biological aging) and showed evidence of more advanced/f

91 .e., genes and molecular pathways that favor biological aging, and alternatively slowed down by geros

92 ological age biomarkers, factors influencing biological aging, and antiaging interventions, with a fo

93 thelium that are known to be associated with biological aging, and cellular senescence markers in HIV

94 gger senescence at a younger age, accelerate biological aging, and drive the initiation or progressio

95 ociations between combined SDHs, accelerated biological aging, and health outcomes.

96 Telomere length (TL) is a marker of biological aging, and numerous studies have shown associ

97 and are associated with decreased lifespan, biological aging, and poorer clinical outcomes.

98 sights into interactions among genetic risk, biological aging, and sex differences in LOAD are presen

99 Telomere length (TL) is a marker of biological aging, and shorter telomeres have been associ

100 e whether MDD is associated with accelerated biological aging, and whether depression characteristics

101 ion may reflect early detrimental aspects of biological aging, apparent even in children.

102 In children, as in adults, biological aging appears to be a multi-faceted process a

103 Socio-economic status (SES) and biological aging are risk factors for dementia, includin

104 t, ascertaining whether treatment effects on biological aging are short-lived or persistent, and test

105 hronic stress is associated with accelerated biological aging as indexed by short age-adjusted leukoc

106 DNAm) and blood-chemistry quantifications of biological aging as mediators of disparities in healthsp

107 osclerosis is also associated with premature biological aging, as atherosclerotic plaques show eviden

108 Our data do not provide evidence that biological aging, as measured by any of the six epigenet

109 arker of cellular senescence associated with biological aging, as the most highly up-regulated pathwa

110 which chronic psychosocial stress may impact biological aging, as well as the neuroendocrine mediator

111 Biological aging assessed from banked blood DNAm using 1

112 Biological aging assessed from blood DNA methylation usi

113 ic health issues may emerge from accelerated biological aging associated with long-term obesity.

114 Biological-aging-associated risk of depression/anxiety w

115 ent diseases in the United States, caused by biological aging, autoimmune conditions, trauma, or iatr

116 e psychopathology exhibited a faster pace of biological aging (B, 0.27; 95% CI, 0.21-0.33; P < .01);

117 celeration (EAA) is a composite biomarker of biological aging based on DNA methylation measurements;

118 no evidence for salient differences in neuro-biological aging between the two sensory regions, the ob

119 Schizophrenia is accompanied by accelerated biological aging by midlife.

120 Biological aging can be described as accumulative, prolo

121 indings suggest that reducing disparities in biological aging can contribute to building health equit

122 Telomere length (TL), a novel measure of biological aging, can be used as a biomarker of stress.

123 end of chromosomes, which are associated to biological aging, cardiovascular disease, cancer and mor

124 Multi-organ biological aging clocks across different organ systems h

125 Biological aging clocks across organ systems and tissues

126 -organ interconnection, including 24 non-MRI biological aging clocks and 525 disease endpoints.

127 Biological aging clocks produce age estimates that can t

128 The 5 MetBAGs extend existing biological aging clocks to study human aging and disease

129 ed brain aging also demonstrated accelerated biological aging, cognitive decline and increased geneti

130 Modern programmed (adaptive) theories of biological aging contend that organisms including mammal

131 We hypothesize that advanced biological aging contributes to cancer-related morbidity

132 Telomere attrition is a hallmark of biological aging, contributing to cellular replicative s

133 ounted for this association, suggesting that biological aging could be adversely influenced by nonnut

134 If so, measurements of the pace of biological aging could offer intermediate end points for

135 Measures of biological aging could prove valuable for assessing pati

136 Understanding differences in biological aging could ultimately allow clinicians to be

137 the same chronological age varied in their "biological aging" (declining integrity of multiple organ

138 Overall, our study reveals that the biological aging discrepancy partially explains the asso

139 those models to quantify the acceleration of biological aging due to tobacco use.

140 amined whether levels of selected markers of biological aging (e.g., allostatic load, telomere length

141 Biological aging estimators derived from DNA methylation

142 e the potentially enduring impact of loss on biological aging even before middle age and may contribu

143 and [Formula: see text] to tangible marks of biological-aging factors.

144 RIBAGs that enhance the existing multi-organ biological aging framework, and we demonstrate their cli

145 We quantified biological aging from 4 DNAm "clocks" (Horvath, Hannum,

146 onnaires and provided blood samples to index biological aging from DNA methylation data (DunedinPACE,

147 Rationale: Accelerated biological aging has been implicated in the development

148 yndrome, a clinical syndrome associated with biological aging, has not been comprehensively investiga

149 methylation clocks that may mark underlying biological aging, have been implicated in the link betwe

150 challenges, such as transition to adulthood, biological aging, illness, and societal transformation,

151 Senescence or biological aging impacts a vast variety of molecular and

152 experienced from childhood to adulthood and biological aging in a diverse sample of the US populatio

153 n UPF was associated with an acceleration of biological aging in a large sample of Italian adults.

154 l and lifestyle factors were associated with biological aging in a nationally representative cohort o

155 elationship between reproductive history and biological aging in a sample of young (20 to 22yo) men a

156 The rate of biological aging in AD patients, which cannot be explain

157 more generalizable and reliable in assessing biological aging in aging-related diseases and rejuvenat

158 termination and predicting the trajectory of biological aging in an individual.

159 and showed evidence of more advanced/faster biological aging in Black participants than in White par

160 60 Years, p = 0.008), suggesting accelerated biological aging in both cohorts with PTSD.

161 tyle factors were more often associated with biological aging in clocks trained to estimate morbidity

162 ur findings delineate cellular correlates of biological aging in combat-related PTSD, which may help

163 CALE, a statistical pipeline that quantifies biological aging in different tissues using explainable

164 ggest in-utero undernutrition may accelerate biological aging in later life.

165 hile CMV has been associated with markers of biological aging in older adults, including immunosenesc

166 tatin may prevent an increase in the pace of biological aging in PWH and support further research int

167 the intersection of HSCT, inflammation, and biological aging in the context of MM.

168 nking internalizing disorders to accelerated biological aging in the first half of the life course, p

169 c machinery maintenance, and determinants of biological aging in these growth disorders.

170 One factor that could accelerate biological aging in women is reproduction.

171 ubertal years is associated with accelerated biological aging in young adulthood.

172 Measured biological aging in young adults can be used to identify

173 We applied these methods to assess biological aging in young humans who had not yet develop

174 are particularly associated with accelerated biological aging in youths, which may be a mechanism lin

175 at a median age of 28 years) and markers of biological aging, including epigenetic age acceleration

176 posite index and the low correlation between biological aging indicators suggest that one's biologica

177 Correlations between biological aging indicators were small (all r < 0.2), in

178 lth outcomes and may contribute to premature biological aging into adulthood.

179 Biological aging is a distinct construct from health; ho

180 Although aging is an immutable part of life, biological aging is a highly heterogeneous process influ

181 Biological aging is a proposed mechanism through which s

182 Biological aging is accompanied by increasing morbidity,

183 Accelerated biological aging is associated with decreased physical c

184 Biological aging is the gradual, progressive decline in

185 However, biological aging is thought to begin before age-related

186 ionship with telomere length, a biomarker of biological aging, is still limited, with no study availa

187 dolescence to reduce the risk of accelerated biological aging later in life.

188 ed epigenetic age measures have been used as biological aging markers and are associated with a healt

189 ronic stress exposures, stress hormones, and biological aging markers in midlife adults and whether s

190 ross-sectional data suggest that accelerated biological aging may be a mechanism through which sleep

191 study of very preterm neonates suggests that biological aging may be associated with impaired brain g

192 endent of chronological age, suggesting that biological aging may contribute to neurological injury i

193 ited evidence has suggested that accelerated biological aging may play an important role.

194 Advanced biological aging may represent a potential risk factor f

195 Targeting fundamental processes underlying biological aging may represent a yet relatively unexplor

196 ects older adults, individual differences in biological aging may represent an important modifier of

197 Thus, the overproduction of noggin during biological aging may result in impaired osteoblast forma

198 ow NSES was associated with a higher rate of biological aging measured by DunedinPACE score, yet indi

199 We show that increased biological aging (measured using epigenetic data from bl

200 th accelerated development across two global biological aging metrics: DNA methylation (DNAm) age and

201 s that may arise from cumulative patterns of biological aging occurring over the life course.

202 S-mediated DNA damage results in accelerated biological aging of hVSMCs via 2 mechanisms: (1) Acute S

203 cations with adverse child outcomes; altered biological aging of the growing fetus up to birth is one

204 to adverse social conditions may accelerate biological aging, offering one mechanism through which a

205 h older brainAGEs had an accelerated pace of biological aging, older facial appearance, and early sig

206 eloping MDD are characterized by accelerated biological aging, operationalized as shortened telomere

207 esting that TL is not an important marker of biological aging or exposure to environmental stress in

208 r the AHP amplitude is strictly dependent on biological aging or is modified by the training procedur

209 lerated development across global metrics of biological aging or whether this pattern emerges followi

210 flect immune and developmental components of biological aging, our study suggests pathways through wh

211 tor composite score comprising 4 measures of biological aging: pace of aging, gait speed, brain age (

212 A series of chronological and biological aging parameters in XRCC1 heterozygous (HZ) m

213 The search for biomarkers that quantify biological aging (particularly 'omic'-based biomarkers)

214 onic psychosocial stress influences distinct biological aging pathways to alter rates of aging likely

215 etable with reference to a rate of 1 year of biological aging per 1 year of chronological aging.

216 drivers of health inequalities, but whether biological aging plays a role in linking SDHs to health

217 AA measures and incident AF, suggesting that biological aging plays an important role independent of

218 remains unclear whether obesity accelerates biological aging, potentially leading to early-onset chr

219 ations between early life experience and the biological aging process in midlife may contribute to he

220 e impacts of environmental exposures and the biological aging process.

221 ion (PhenoAgeAccel) was used to evaluate the biological aging process.

222 n humans that stress hormones may impact key biological aging processes and may be a mechanism linkin

223 (catecholamines, glucocorticoids) can impact biological aging processes such as DNA damage and cellul

224 s clinical and translational studies to link biological aging processes to underlying ADRD pathogenes

225 to noncommunicable diseases associated with biological aging processes, such as cancer, cardiovascul

226 arch is aimed at their potential to quantify biological aging rates and test longevity or rejuvenatin

227 However, within populations, biological aging rates vary.

228 modynamic factor as independent predictor of biological aging, rather than a simple confounding varia

229 enetic age provides a reliable biomarker for biological aging, reflecting the cumulative impact on he

230 each new patient was on a distinct course of biological aging related to past exposures, life experie

231 discussion on possible future directions in biological aging research using deep learning.

232 immense opportunities in the field of human biological aging research.

233 oxidative modification of CaM during normal biological aging results in a reduced calcium sensitivit

234 CH may be an independent biological aging risk factor contributing to inferior su

235 Also, accelerated biological aging served as a mediator between SDHs and i

236 Most of the variation in biological aging shared with adolescent lifestyle was ex

237 Genetic and environmental influences on biological aging shared with lifestyle behavior patterns

238 Accelerated biological aging significantly mediated the association

239 reased molecular markers of inflammation and biological aging suggests their potential to modify aspe

240 esents a conceptual framework of life course biological aging, summarizes candidate measures, and des

241 .07 (0.14), representing a 7% faster pace of biological aging than chronological aging.

242 Telomere length is a marker of biological aging that may provide a cellular memory of e

243 During the course of biological aging, there is a gradual accumulation of dam

244 tions on pubertal development and ultimately biological aging, these findings highlight the importanc

245 EAA measures biological aging through DNA methylation patterns and ma

246 developed a mathematical model that defines biological aging through two parameters, eta and [Formul

247 clocks allow for quantitative estimation of biological aging trajectories.

248 We quantify biological aging using six measures, collectively known

249 when the survivors were aged 58 to quantify biological aging using the DunedinPACE, GrimAge, and Phe

250 al discrimination contributes to accelerated biological aging via altered connectivity between the LC

251 rsistent infections, particularly CMV, shape biological aging via DNA methylation aging and immunosen

252 Biological aging was also measured using epigenetic meth

253 The pace of biological aging was measured from whole-blood DNA-methy

254 enescence/exhaustion that is associated with biological aging, was positively correlated with AgeAcce

255 ltaage = BA - chronological age)-an index of biological aging-was tested as dependent variable in mul

256 early-life adversity accelerates the pace of biological aging, we analyzed data from the Dutch Hunger

257 The most consistent associations of advanced biological aging were found for male sex, higher body ma

258 DNAm and blood-chemistry quantifications of biological aging were moderately correlated (Pearson's r

259 d differences between the subgroups in later biological aging were studied.

260 ted a U-shaped relationship with accelerated biological aging when controlling for chronological age,

261 generate DNA methylation-based biomarkers of biological aging, which may be useful in predicting a my

262 eriodontitis could modify the association of biological aging with all-cause and cause-specific morta

263 riodontitis might enhance the association of biological aging with all-cause mortality in middle-aged

264 ed DNA methylation (DNAm) was used to assess biological aging with six epigenetic aging measures in y