ライフサイエンスコーパス: aging

1 ng stress (DNA damage, targeted therapy, and aging).

2 ystem from changes associated with premature aging.

3 c disorders, neurodegenerative diseases, and aging.

4 nctional decline is a visible consequence of aging.

5 y distinct phases of airway regeneration and aging.

6 essful repair, and kidney homeostasis during aging.

7 ocal and systemic effects on host health and aging.

8 th (LTL) is a heritable biomarker of genomic aging.

9 melioration of both somatic and reproductive aging.

10 gy by knocking down WIPI2 suffices to induce aging.

11 be extended to other LMICs facing population aging.

12 e effects of aggregation leading to in vitro aging.

13 Telomere shortening is a hallmark of aging.

14 phenotype that is alarmingly increased with aging.

15 ve been associated with accelerated cellular aging.

16 e to no benefit for other common symptoms of aging.

17 the fields of neurodegeneration, cancer and aging.

18 for treatments for diseases associated with aging.

19 elioration of neurodegenerative diseases and aging.

20 inflammation and cellular senescence during aging.

21 arrel, raw material, distillation method and aging.

22 tion to prevent cognitive decline in healthy aging.

23 e, yet chronically elevated with obesity and aging.

24 primary non-autonomous mechanism for cardiac aging.

25 s been established as a hallmark of nematode aging.

26 inflammation-resolution and efferocytosis in aging.

27 use is a well-established model of premature aging.

28 ack with age, but also relates to phenotypic aging.

29 blasts functions as a key mediator of dermal aging.

30 lomere length, a proposed biomarker of human aging.

31 signaling as therapeutic targets for cardiac aging.

32 eins in the dermal fibroblast secretome with aging.

33 in ECM biology, wound healing, diseases, and aging.

34 eatment, and UI is not an inevitable part of aging.

35 midlife may help reduce cognitive decline in aging.

36 isiae accumulate lipid droplets (LDs) during aging.

37 reduce depression and contribute to healthy aging.

38 nnected hallmark processes driving mammalian aging.

39 alence of periodontal disease increases with aging.

40 mesenchymal stromal/stem cells (MSCs) during aging.

41 re for aging adults would promote successful aging.

42 n the immune system to modify the process of aging.

43 ghting requirements for brain homeostasis in aging.

44 gulation and the decay of muscle function in aging.

45 identified in alveolar bone osteocytes with aging.

46 development, with limited changes in healthy aging.

47 processes change over the course of healthy aging.

48 aces has been proposed as an explanation for aging.

49 ration and hence is unlikely to be causal in aging.

50 In contrast, aging (18-24-month-old) Carns1-deficient mice exhibited

51 Aging (5 vs 12 mo) and/or compression reduced the transc

52 ith ESKD and more thoughtful health care for aging adults would promote successful aging.

53 Furthermore, we identified that aging alters Sirtuin-1-hepatic nuclear factor 4alpha cir

54 ured by antioxidant capacity may retard skin aging among healthy men and women aged >45 years.

55 understanding of the molecular regulation of aging and age-related diseases is still in its infancy,

56 This is relevant in aging and age-related neurological diseases, where neuro

57 standing and studying the mechanisms of skin aging and age-related skin disorders.

58 mal models, which incorporate the effects of aging and associated comorbid conditions; (2) repositori

59 Despite their relevance for understanding aging and cancer, the processes that underpin mutational

60 age commitment that may have implications in aging and cancer.

61 hat protein aggregation is a major driver of aging and cell death during growth arrest, and that coor

62 l transcriptional landscapes associated with aging and CR in a mammal, enhances our understanding of

63 We consider how co-morbidities related to an aging and damaged soma can hinder achievement of ACM ben

64 tober 2018]; and Translational Biomarkers in Aging and Dementia [TRIAD, n = 116; 74 cognitively unimp

65 osis patients, demyelination progresses with aging and disease course, leading to irreversible disabi

66 y number that result in organ dysfunction in aging and disease have often not been clarified.

67 t to cellular processes and how these impact aging and disease.

68 ght into their possible causal role in human aging and disease.

69 avel the role of mitochondrial plasticity in aging and disease.

70 hippocampal memory updating is impaired with aging and establish that the OUL paradigm is an effectiv

71 pathway gene, reduces LD accumulation during aging and extends lifespan.

72 ffect senescence across species with diverse aging and fertility schedule phenotypes.

73 We next asked how aging and functional self-assembly influence these solub

74 The stronger relationship between aging and GCL thickness compared with the rim or peripap

75 We identified widespread cell-type-enriched aging and genetic effects in the DG-GCL that were either

76 ed signatures, allowing modeling of vascular aging and HGPS in vitro.

77 However, how it is affected by aging and how this in turn impacts cell function remains

78 f the important role the microbiome plays in aging and how this knowledge opens the door for potentia

79 s herpes zoster, a major health issue in the aging and immunocompromised populations.

80 o control disease, with a connection between aging and impaired adaptive immune responses to SARS-CoV

81 view, we discuss roles for the microbiome in aging and in NDs.

82 and loss of miR-146a promoted premature HSC aging and inflammation in young miR-146a-null mice, prec

83 gestive of a mechanistic convergence between aging and lysosomal storage disorders.

84 n diverse cancer-related hallmarks including aging and metabolic alterations, but its impact on liver

85 ation to counter functional decline in brain aging and neurodegeneration.

86 zed by neuronal mitochondria, decreases with aging and neurodegeneration.

87 of the human brain are implicated in typical aging and neurodegenerative diseases.

88 PK or p53 prevents or rescues ISC and villus aging and nutrient absorption defects.

89 Both aging and obesity are characterized by profound systemic

90 in various inflammatory conditions including aging and obesity.

91 ) sequence and copy number are implicated in aging and organ dysfunction in diverse inherited and spo

92 diseases, which have features of accelerated aging and osteoporosis.

93 ulating cf-mt-DNA as a key factor in inflamm-aging and present senolytics as a potential approach to

94 Women's Health Initiative Study of Cognitive Aging and the Women's Health Initiative Memory Study of

95 r life reflects both influences of intrinsic aging and those of lifestyle, environment and disease.

96 proaches may be developed to balance between aging and tumor suppression, for example, by differentia

97 s on the neural underpinning of attention in aging and underscore the importance of the noradrenergic

98 UPR and DDR alterations are associated with aging and with pathologies such as degenerative diseases

99 yonic retinal progenitors for the effects of aging and, independently, of retinal environment age on

100 e biomarkers, factors influencing biological aging, and antiaging interventions, with a focus on vasc

101 dual participant-level data from the Health, Aging, and Body Composition Study, the Multi-Ethnic Stud

102 women (n = 1237) aged 70-81 y of the Health, Aging, and Body Composition Study.

103 rom the Finnish Cardiovascular Risk Factors, Aging, and Dementia (CAIDE) study, who were followed fro

104 I have been involved in studies of cognitive aging, and I describe some theoretical and empirical poi

105 t can be altered by environmental exposures, aging, and in pathogenesis.

106 on, cognition, pain, metabolic function, and aging, and in so doing potentially increasing the risk o

107 tal anomalies, maternal/reproductive health, aging, and infection were identified as important for in

108 tanding the complex interplay between Abeta, aging, and neurodegeneration within the most vulnerable

109 ein could be linked to nutrient stress, cell aging, and subsequent production of substances that prom

110 ty in TMJ osteoarthritis (OA) increases with aging, and the main goal is to diagnosis before morpholo

111 Aging appears to attenuate the response of skeletal musc

112 The molecular changes that occur with aging are not well understood(1-4).

113 How lifespan and the rate of aging are set is a key problem in biology.

114 gest that it is important not to treat brain aging as a single homogeneous process, and that modellin

115 s, receptors, and/or pathways that influence aging as well as the individual or groups of neurons inv

116 We discovered additional changes in aging, as glandular-like epithelial invaginations (GLEIs

117 ver, the cellular profiles and signatures of aging, as well as those ameliorated by CR, remain unclea

118 g-associated neuroinflammation and alleviate aging-associated cognitive decline.

119 ldehyde-driven mutation signature similar to aging-associated human cancer mutation signatures.

120 Thus, in both diet- and aging-associated hyperinsulinemia, excessive Insr signal

121 Aging-associated inflammation, telomere dysfunction, and

122 de 1-42 (Abeta(42)) stimulation in vitro, in aging-associated microgliosis in vivo and in post-mortem

123 miR-146a-null mice, preceding development of aging-associated myeloid malignancy.

124 ajor ILC2 product, was sufficient to repress aging-associated neuroinflammation and alleviate aging-a

125 At the chromatin level, aging associates with progressive accumulation of epigen

126 ecific mechanisms underlying primate ovarian aging at single-cell resolution, revealing new diagnosti

127 lera aging method, use of different types of aging barrels) on several parameters: color, non-enzymat

128 nzymes and has been implicated in cancer and aging because of its role as a global epigenetic modifie

129 Objective: To determine if vascular aging before the induction of hyperlipidemia enhances at

130 cohort, the Baltimore Longitudinal Study of Aging (BLSA).

131 ngs to neurodegenerative diseases and in the aging brain.

132 erences in white matter condition across the aging brain.SIGNIFICANCE STATEMENT Age-associated defici

133 he ejaculate contribute to male reproductive aging but reveal a mismatch in their aging patterns.

134 lavanol-rich diets protect against cognitive aging, but mechanisms remain elusive.

135 Brain aging can be modeled statistically; the so-called "brain

136 methyl-2,4-nonanedione (MND) during red wine aging can contribute to the premature evolution of aroma

137 (BB) emits organic gases that, with chemical aging, can form secondary organic aerosol (SOA) in both

138 , OOC-5, rescues the sterility and premature aging caused by a null mutation in the single worm lamin

139 Here we evaluated whether premature aging caused by accumulation of mitochondrial DNA mutati

140 nalyses of genome-wide methylation levels in aging cells.

141 RPD were seen in 2.4% of eyes with no AMD or aging changes, 11.5% in early AMD, 25.1% in intermediate

142 were possibly important for defining unique aging characteristics of certain vineyards.

143 circulating neutrophils undergo a process of aging characterized by loss of surface CD62L and upregul

144 At baseline, a decade of chronological aging correlated with a decrease in Ao-A, Ao-P, and Ao-D

145 Cognitive aging creates major individual and societal burden, moti

146 have increased over time, associated with an aging demographic.

147 However, the impact of the aging dermal environment on female scalp hair follicles

148 Our results indicate that healthy aging does not significantly impair simple reinforcement

149 Theoretical models for the aging dynamics need to be revised accordingly.

150 aking takes place in mean-field spin glasses aging dynamics which, asymptotically, takes place in a c

151 radicals in the human body, showing an "anti-aging" effect in high-voltage battery cycling and succes

152 We determined the differential aging effects of the inner 6 layers of the macula in con

153 ndo treated with selenium, a well-known anti-aging element to capture oxygen-radicals in the human bo

154 , which revealed a dynamic adaptation of the aging female brain from glucose centric to utilization o

155 led by bioenergetic dysregulation in midlife aging female brain.

156 Mimicking the effect of advanced aging, genetic disruption of lysosomal function accelera

157 ic Epidemiology Research on Adult Health and Aging (GERA) cohort and 5467 subjects aged 2 to 26 years

158 However, spontaneous rates were decreased in aging gerbils.

159 In the non-aging H. vulgaris animals, the blockade of autophagy by

160 ipoprotein (a) [Lp(a)] and healthy cognitive aging has not yet been sufficiently investigated.

161 Surprisingly, although numbers declined, aging HFSCs were present, maintained their identity, and

162 c-specific mass spectrometry analysis of the aging hippocampus, together with an in vitro site-direct

163 Aging HIV-infected (HIV+) men who have sex with men (MSM

164 ression heterogeneity is a characteristic of aging human brain, and may influence aging-related chang

165 We tested for three key features of HPA aging identified in many human studies: increased averag

166 have a selective advantage and accumulate in aging IJs in advance of exposure to insect hosts in whic

167 lating diverse biological phenomena, such as aging, immunity, proteostasis and programmed cell death.

168 We report that aging impairs the expression of Gadd45gamma in the hippo

169 of a simple interdependent network model of aging in complex systems and show that it exhibits casca

170 Needs of the Elderly Population for Healthy Aging in Europe (NU-AGE)] was carried out in older Europ

171 ore biologically meaningful markers of brain aging in health and disease.

172 evolutionary context for patterns of social aging in humans.

173 ' reproductive decline, an early hallmark of aging in many animals.

174 an rescue cognitive deficits associated with aging in mice.

175 buildup of lipid droplets in microglia with aging in mouse and human brains.

176 nd MMP13 were significantly upregulated with aging in osteocyte-enriched samples.

177 g of the neural mechanisms of neurocognitive aging in our own species.

178 y understand the impact of BMI on epigenetic aging in sperm.

179 A better understanding of the hallmarks of aging in the liver will be crucial in the development of

180 fectively combats the deleterious effects of aging in the musculoskeletal system, how long-term exerc

181 ncer point to the significance of epigenetic aging in tumorigenesis and its potential use for cancer

182 Normal aging, in the absence of dementia, also results in gradu

183 -cell communication patterns observed during aging, including the excessive proinflammatory ligand-re

184 ltiple sclerosis (MS) attributable to normal aging increased from 42.7% and 16.7% respectively at age

185 the lifespan or sustain the impacts of brain aging independently.

186 armacy purchase and mortality data of 12,047 aging individuals.

187 Since sestrin also protected muscles against aging-induced atrophy, our findings have implications fo

188 novel mechanism, and therapeutic target, for aging-induced essential hypertension in humans.

189 e results suggest that older molecular brain aging is a common feature of severe mental illnesses and

190 Cellular aging is a multifactorial process that is characterized

191 f insulin secretion and identify how granule aging is affected by variation in the beta-cell environm

192 macronutrient intake, and whether epigenetic aging is associated with cardiovascular health markers i

193 Aging is associated with defective inflammation-resoluti

194 Aging is associated with inflammation and metabolic synd

195 Natural lung aging is associated with molecular and physiological cha

196 Brain aging is associated with molecular, cellular, and struct

197 Aging is associated with significant changes in the hema

198 Aging is characterized by a gradual loss of function occ

199 ogeronic and antigeronic factors in vascular aging is discussed.

200 genes and interventions that slow or reverse aging is hampered by the lack of non-invasive metrics th

201 Mechanistically, this LD accumulation during aging is not linked to NAD(+) levels, but is anti-correl

202 However, the role of sex in immune system aging is not well understood.

203 tration-dependent phase separation, which on aging is rationalized in a decrease of their effective s

204 essive illumination, inherited mutations, or aging is the principal pathology of blinding diseases.

205 A prominent molecular process underlying aging is the progressive shortening of telomeres, the st

206 euronal and cognitive function during normal aging is underexplored.

207 sosome surface, increased lysosome mass with aging leads to higher mTORC1 activity.

208 wild type, disease-free mice and found that aging led to elevated IL (interleukin)-6 levels and mito

209 Dimensions of the aging lens vary considerably and are most accurately cha

210 evented excess steatosis and inflammation in aging livers but did not reduce the number of CD11b(+) m

211 and consequences of visual impairment among aging long-term survivors of HIV.

212 cal, structural, and cellular changes in the aging lung and immune system that facilitate the develop

213 ers of cellular senescence that overlap with aging markers in human plasma, including Growth/differen

214 e origins and accumulation of mutations with aging/maturation and has implications for delayed reprod

215 These findings suggest that aging may alter neural processes for segmenting and reme

216 Reproductive aging may contribute to cardiometabolic comorbid conditi

217 In the context of population aging, MDS incidence is set to increase substantially, w

218 Our results implicate vHMM-HA in anti-aging mechanisms and suggest the potential applications

219 is among the most common diseases affecting aging men, but the underlying molecular features remain

220 ion, addition of additives or spices, solera aging method, use of different types of aging barrels) o

221 05 for the treatment of cognitive deficit in aging mice.

222 is review focuses on cGAS-STING signaling in aging, neurodegeneration, and neuroinflammation, and on

223 be upregulated by activated microglia during aging, neurodegeneration, or loss of Sall1.

224 cations of cysteines during inflammation and aging, no systematic comparative study of potential dire

225 (edges)| = .583), suggesting that connectome aging occurs on broad dimensions of variation in brain a

226 In this study, the aging of BB tar proxy aerosols processed by NO(3)(*) und

227 at determines which process dominates during aging of individual cells is unknown.

228 mice, is stabilized at low levels during the aging of long-lived NMRs and bats.

229 Accompanying the aging of populations worldwide, and increased survival w

230 = 8185; age range, 45-78 years), we examined aging of regional gray matter volumes (nodes) and white

231 tein damage, which is substantial during the aging of short-lived mice, is stabilized at low levels d

232 he Muller's ratchet principle applied to the aging of somatic cell populations and discuss the implic

233 a transition of these two cell fates during aging of telomerase deficient zebrafish.

234 However, modeling healthy and pathological aging of the human vasculature represents an unresolved

235 biological actions, and how it misbehaves in aging or disease.

236 ductive aging but reveal a mismatch in their aging patterns.

237 alence of neurocognitive impairment (NCI) in aging people living with human immunodeficiency virus (P

238 ld contribute to the premature immunological aging phenotype observed in these patients.

239 for future approaches designed to thwart the aging phenotype.

240 These aging phenotypes are recapitulated in intestinal stem ce

241 esults demonstrate that pre-existing cardiac aging phenotypes can be reversed by targeting mitochondr

242 combinant GDF11 (rGDF11) to aged mice alters aging phenotypes in the brain, skeletal muscle, and hear

243 US Latinos, a growing, aging population, are disproportionately burdened by cog

244 eurobiological bases of cognitive decline in aging populations may provide critical insights into the

245 ecause of its involvement in both the normal aging process and common human diseases.

246 ons, with a focus on vascular aspects of the aging process and its cardiovascular disease related man

247 c and treatment strategies that may slow the aging process based on the unique biochemistry of each i

248 existing pipelines to better understand the aging process.

249 Klotho is downregulated as part of the aging process.

250 es over a lifetime as part of an "epigenetic aging" process.

251 ts in the Washington Heights-Inwood Columbia Aging Project (WHICAP).

252 e cellular and molecular intricacies of skin aging provide a foundation for future approaches designe

253 o not find any consistent sex differences in aging rates.

254 Aging-related cellular and molecular processes including

255 stic of aging human brain, and may influence aging-related changes in brain functions.

256 CR attenuated aging-related changes in cell type composition, gene exp

257 ed single-cell RNA-sequencing to interrogate aging-related changes in the HFSCs.

258 eritable diseases, acquired pathologies, and aging-related declines in health.

259 ted with an increased risk of brain atrophy, aging-related diseases, and mortality.

260 s for progress in molecular understanding of aging-related disorders and neurodegenerative diseases.

261 ociated with increased life span and reduced aging-related disorders and reduces fibrosis in several

262 mics and functional significance of putative aging-related heterogeneity are also unknown.

263 nuclear and cytosolic sirtuin inhibition to aging-related inflammatory disease development.

264 rget of cellular stress, toxin exposure, and aging-related injury.

265 ent firing capacity, which may contribute to aging-related learning impairments.

266 oteasome inhibition within neurons, to mimic aging-related reduction of proteasome activity, induced

267 ogy and function, and their breakdown during aging, remain unclear.

268 that protects against metabolic diseases and aging, represses cancer growth and improves cancer thera

269 Understanding human skin aging requires in-depth knowledge of the molecular and f

270 by profound structural perturbations in the aging SC niche.

271 mechanism underlying the link between muscle aging/senescence and osteoporosis.

272 s mediated by nAChRs may be compromised with aging.SIGNIFICANCE STATEMENT When attention is required,

273 Aging significantly changes the ability to respond to va

274 m fresh (<1 day of aging) to old (>3 days of aging) smoke.

275 rly-life risk factors for newborn epigenetic aging, specifically maternal dietary macronutrient intak

276 osheet layers and unveiled the heterogeneous aging state of MoS(2) nanosheets.

277 lucanase action, respectively, and peaked in aging, strengthening tissues: CXE in xylem and cells bor

278 f how to maximize health and longevity in an aging system at minimal cost of maintenance and interven

279 crucial component of the mitochondrial anti-aging system.

280 s and mechanisms that underlie microvascular aging, the greatest risk factor for cerebrovascular dise

281 With aging, there is a loss of hemispheric asymmetry in neuro

282 ly damaged DNA has been linked to cancer and aging, therefore it is of great interest to map DNA dama

283 CR moderates intrinsic processes of aging through cellular and metabolic adaptations and red

284 on metabolism and the circadian system with aging through the spatiotemporal control of the molecula

285 n Spain were analyzed to study the effect of aging time and manufacturing steps (filtration, addition

286 t their OCR tended to decrease with the wine aging time.

287 t ER stress as a potential mechanism linking aging to IPF.

288 smoke age by up to 72% from fresh (<1 day of aging) to old (>3 days of aging) smoke.

289 t the use of proteomic biomarkers to monitor aging trajectories and to identify individuals at higher

290 We examined aging trajectories of cortical thickness (CTh) and surfa

291 The chimpanzee aging trajectory compared with the human trajectory was

292 d network stability as a biomarker for brain aging using two large-scale (n = 292, ages 20 to 85 y; n

293 Klotho deficiency causes cardiac aging via impairing the Nrf2-GR pathway.

294 Healthy aging was characterized by decreased static resting-stat

295 and somatosensory systems deteriorate during aging, we aimed to: (1) compare the effects of footwear

296 identify metabolic pathways associated with aging, we analyzed age-dependent changes in the metabolo

297 em, how long-term exercise affects stem cell aging, which is typified by reduced proliferative and di

298 echnology to address the overwhelming global aging, which requires advanced micro power sources with

299 visualized in renal tubules as a function of aging, which was prevented by calorie restriction.

300 cesses, that are generally intact in healthy aging, will be particularly compromised in people at the