ライフサイエンスコーパス: aging-related

1 We predict such genes to be aging-related.

2 expression reversals may be associated with aging-related accumulation of stochastic effects that le

3 dipocytes is a hallmark of adipose aging and aging-related adipose dysfunction.

4 s of SIRT2 reduces AMPK activation, promotes aging-related and Ang II-induced cardiac hypertrophy, an

5 e aimed to investigate the roles of SIRT2 in aging-related and angiotensin II (Ang II)-induced pathol

6 In contrast, human OA and aging-related and surgically induced OA in mice are asso

7 ar cartilage and in knee joints of mice with aging-related and surgically induced OA, using immunohis

8 e TNF receptor-1 gene (TNFR1) contributes to aging-related atherosclerosis in humans and whether Tnfr

9 mans and whether Tnfr1 expression aggravates aging-related atherosclerosis in mice.

10 of the basal forebrain, which later develop aging-related atrophy and degenerative changes, as in AD

11 Elevated rate of aging-related biological and functional decline, termed

12 s rather than enhance the expression of skin aging-related biomarkers ex vivo.

13 Aging-related bone loss and osteoporosis affect millions

14 urons is an attractive approach for modeling aging-related brain disorders.

15 ntracellular Ca(2+) responses, reverses both aging-related Ca(2+) dysregulation and cognitive impairm

16 g FKBP1b is a molecular mechanism underlying aging-related Ca2+ dysregulation and unhealthy brain agi

17 lude that TNFR1 polymorphisms associate with aging-related CAD in humans, and TNFR1 contributes to ag

18 In tissues susceptible to aging-related cancers, including the prostate, a relaxat

19 diates canonical Wnt signaling, for roles in aging-related cardiac dysfunction.

20 mice were subjected to the investigation of aging-related cardiac hypertrophy.

21 ves play key roles in cardiac physiology and aging-related cardiovascular diseases.

22 e (NTPPPH) activity are strongly linked with aging-related cartilage calcification in meniscal and ar

23 signaling interaction is a new mechanism in aging-related cartilage pathology.

24 Mechanisms leading to the aging-related cartilage surface degeneration remain to b

25 on the efficacy of glucosamine in modifying aging-related cellular changes and supporting joint heal

26 better understanding the molecular basis of aging related changes in neuroendocrine stress systems.

27 nces in the incidence of hypertension and in aging-related changes in blood pressure by neighborhood

28 ued progress is being made on characterizing aging-related changes in cartilage.

29 us, this study reveals a novel mechanism for aging-related changes in CD8 T cells.

30 In sum, we have identified aging-related changes in cTfh that correlated with reduc

31 current studies were performed to determine aging-related changes in polymorphonuclear neutrophil (P

32 These results support the concept that aging-related changes in the prostate microenvironment m

33 ort the identification of genes that exhibit aging-related changes of mRNA levels.

34 ss questions concerning genetic influence on aging-related characteristics.

35 go a transition to beta-sheet as a result of aging-related chemical modifications of aspartyl residue

36 tress, has increased activity with aging and aging-related chronic diseases.

37 l cortex, an area previously associated with aging-related cognitive changes, is critical for normal

38 E (apoE) is a strong genetic risk factor for aging-related cognitive decline as well as late-onset Al

39 n changes in white matter microstructure and aging-related cognitive decline during the eighth decade

40 One contributor to aging-related cognitive decline is decreased intrinsic e

41 Understanding aging-related cognitive decline is of growing importance

42 ociated with pathological features of AD and aging-related cognitive decline.

43 Aging-related cognitive declines are well documented in

44 e that a reduction in neurogenesis underlies aging-related cognitive deficits and impairments in diso

45 w way to fight mild cognitive impairment and aging-related cognitive deterioration.

46 and increased glial activation, resulting in aging-related cognitive dysfunction.

47 nflammation in glia that cumulatively induce aging-related cognitive impairment.

48 f health-promoting substances by adults with aging-related cognitive or physical disorders.

49 ty associated with IIM may be complicated by aging-related comorbidities and decreased physical activ

50 Shortened LTL is observed in a host of aging-related complex genetic diseases and is associated

51 c disorders as well as neurodegenerative and aging-related conditions that are associated with loss o

52 rominent with advancing age, suggesting that aging-related cortical demyelination contributes to incr

53 ange rates and extrapolated to further adult aging-related cortical thinning.

54 tive effect of GR levels associated with the aging-related cumulative characteristics of periodontal

55 s, presumably by slowing the accumulation of aging-related damage.

56 nd those that are enriched in 'ground truth' aging-related data; (iii) providing evidence that diseas

57 Center, moderate CR lowered the incidence of aging-related deaths.

58 treatment (acute vs chronic) and whether the aging-related decline in a particular cognitive process

59 ver, the molecular mechanisms underlying the aging-related decline in cardiac muscle function are lar

60 umans as well as other mammals experience an aging-related decline in drug metabolism as well as a di

61 Smoking may accelerate the aging-related decline in glomerular filtration rate.

62 fractional anisotropy (FA) as a biomarker of aging-related decline in white matter (WM) integrity to

63 uggesting that TRAP exposures may accelerate aging-related declines in health.

64 tests of motor coordination, and both showed aging-related decreases in the size of the dopaminergic

65 hogen-derived products, had little effect on aging-related defects in NK cell priming.

66 ding DNA damage, is thought to contribute to aging-related degenerative changes, but how damage drive

67 ogy of aging, as well as the pathogenesis of aging-related degenerative diseases.

68 ss and telomere shortening/dysfunction cause aging-related degenerative pathologies and increase canc

69 Cerebral myelin maturation and aging-related degradation constitute fundamental feature

70 cyte telomere length (LTL) is a predictor of aging-related disease and decreases with each cell cycle

71 this repair mechanism very likely increases aging-related disease susceptibility.

72 ecific stem cells in homeostasis, aging, and aging-related disease.

73 as an attractive therapeutic target for many aging related diseases, however, how its activity can on

74 enous sources, creating lesions that lead to aging related diseases, including cancer.

75 ng because its shortening is associated with aging-related diseases and early mortality.

76 pro-inflammatory cytokines, contributing to aging-related diseases and morbidity.

77 a new therapeutic approach for obesity- and aging-related diseases associated with mitochondrial dys

78 t studies are identifying pathways for these aging-related diseases by examining how the process of a

79 ll telomere attrition predicts mortality and aging-related diseases in inherited telomere syndrome pa

80 ith accelerated aging and increased risk for aging-related diseases, but the underlying molecular mec

81 se risks of cardiovascular disease and other aging-related diseases, but their relationships with leu

82 l inhibitors of SIRT2, an enzyme involved in aging-related diseases, e.g., neurodegenerative disorder

83 prevent telomere-associated diseases, namely aging-related diseases, including cancer.

84 omere shortening has been linked to multiple aging-related diseases, including cancer.

85 ulated genes showed enriched association for aging-related diseases, including coronary artery diseas

86 Because TL plays a significant role in aging-related diseases, insight into the factors that fa

87 s have beneficial effects in metabolism- and aging-related diseases.

88 promising strategy to prevent and alleviate aging-related diseases.

89 g genes associated with human autoimmune and aging-related diseases.

90 umulation, and aggregation characterize many aging-related diseases.

91 nd that LTL is relatively short in a host of aging-related diseases.

92 ated pathways involved in the development of aging-related diseases.

93 etic tools for studying vertebrate aging and aging-related diseases.

94 induction and perpetuation of metabolic and aging-related diseases.

95 stress, abnormalities of which underlie many aging-related diseases.

96 and stress responses, and are implicated in aging-related diseases.

97 rotein in cells is associated with aging and aging-related diseases; however, the roles of insoluble

98 logy in humans and may provide insights into aging-related disorders linked to altered LTL dynamics.

99 ution (DPD) can slow the progression of some aging-related disorders, whether this strategy affects t

100 therapeutic strategies to delay the onset of aging-related disorders.

101 n joint disease and typically begins with an aging-related disruption of the articular cartilage surf

102 molecular evolution rates and predicting new aging-related drugs based on drug-gene interaction data.

103 The dichotomy of learning-related and aging-related effects on two very similar calcium-depend

104 Gpx1 Tg mice were protected from this aging-related enhanced susceptibility to venous thrombos

105 far, many microarray studies have addressed aging-related expression patterns in multiple organisms

106 The combination of 2 aging-related factors (ie, decline in both the mass and

107 here has been steady progress in identifying aging-related factors such as reactive oxygen species an

108 s study, we describe a strategy for inducing aging-related features in human iPSC-derived lineages an

109 re-related FEV(1) decrement equaled 12 yr of aging-related FEV(1) decline.

110 Aging-related functional NK cell deficiency is well docu

111 Finally, we found that aging-related functional NK cell deficiency was complete

112 the aged host environment is responsible for aging-related functional NK cell deficiency.

113 tor agonists may be useful tools in treating aging-related functional NK cell deficiency.

114 MicroRNAs (miRNAs) control aging-related functions such as metabolism and lifespan

115 Moreover, the idea of aging-related gains in wisdom is consistent with views o

116 Because the mRNA level of the senescence (aging)-related gene was significantly elevated in sample

117 sights, we integrate current static BNs with aging-related gene expression data to construct dynamic

118 Genes that changed with aging [aging-related genes (ARGs)] were identified in each regi

119 ng significant overlap between our predicted aging-related genes and 'ground truth' aging-related gen

120 o-longevity genes, revealing new insights on aging-related genes as a whole and their interactions wi

121 First, by classifying aging-related genes as pro- or anti-longevity, we define

122 tified 24 novel but well-supported candidate aging-related genes for further experimental validation.

123 ive set of network characteristics for human aging-related genes from the GenAge database.

124 Although some individual aging-related genes have been the subject of intense scr

125 of aging and the effects of perturbing known aging-related genes on lifespan and behavior.

126 ated diseases are due to a small fraction of aging-related genes which also tend to have a high netwo

127 Our subsequent comparison of aging-related genes with age-related disease genes revea

128 he gerontome across species, including human aging-related genes.

129 icted aging-related genes and 'ground truth' aging-related genes; (ii) observing significant overlap

130 er adults who are potentially susceptible to aging-related health conditions; however, the manifestat

131 Considering the aging-related health risks that the centenarians have su

132 ng hypotheses about causes and treatment for aging-related hepatic changes.

133 ein we performed a biophysical separation of aging-related high molecular weight aggregates, isolated

134 e hypothesis that declining FKBP1b underlies aging-related hippocampal Ca2+ dysregulation.

135 ons have been postulated to account for many aging-related immune dysfunctions.

136 rts the hypothesis that the primary cause of aging-related impairment of muscle function is a cumulat

137 elevated levels of superoxide contribute to aging-related impairments in hippocampal LTP and memory,

138 Aging-related impairments in hippocampus-dependent cogni

139 An aging-related increase was found in high-threshold Ca an

140 rat hippocampal slice CA1 neurons have found aging-related increases in long-lasting calcium (Ca)-dep

141 40% caloric restriction (CR) did not exhibit aging-related increases in oocyte aneuploidy, chromosoma

142 Aging-related increases in systolic blood pressure were

143 ing in both age groups, only the sAHP showed aging-related increases.

144 (iNOS) expression, which are associated with aging-related inflammation and insulin resistance.

145 ring islet regeneration, is depressed during aging-related islet dysfunction, and may be important in

146 Osteoarthritis (OA), the most prevalent aging-related joint disease, is characterized by insuffi

147 fic calpain inhibition would protect against aging-related lesions in arteries and kidneys.

148 itical need for rapid model systems to study aging-related liver changes.

149 by memory CD8(+) T cells, which exhibited an aging-related loss in binding of NF-kappaB and STAT fact

150 SIRT1 agonist can restore this aging-related loss of cardioprotection.

151 In human and murine cartilage, there is an aging-related loss of HMGB2 expression, ultimately leadi

152 To understand if this results in aging-related loss of immune protection against emerging

153 In OA they display aging-related loss of proliferation but no gross osteoge

154 ot restricted to IPF and also occur in other aging-related lung disorders, primarily chronic obstruct

155 ent decreased accumulation of lipofuscin, an aging-related marker, in the brain and enhanced proteaso

156 ved fibroblasts and neurons induces multiple aging-related markers and characteristics, including dop

157 the aging brain, and provide a link between aging-related molecular changes and functional decline.

158 However, evaluations of aging-related mtDNA mutations in other model animal syst

159 n young adult mice, and remarkably, prevents aging-related muscle changes in old adult mice, resultin

160 RET may have a stronger effect in preventing aging-related muscle mass attenuation and leg strength l

161 and the molecular mechanisms underlying this aging-related network specificity, we also analyzed prot

162 oth the aging process and the development of aging-related neurodegenerative brain diseases.

163 onic microinflammation is a hallmark of many aging-related neurodegenerative diseases as well as meta

164 ylated tau, are a common feature of numerous aging-related neurodegenerative diseases, including Alzh

165 ways also modulate fundamental mechanisms in aging-related neurodegenerative diseases, including prot

166 or factor contributing to the development of aging-related neurodegenerative diseases, notably Alzhei

167 uleus (LC) neurons is a prominent feature of aging-related neurodegenerative diseases, such as Parkin

168 evelopment of a therapeutic approach against aging-related neurodegenerative disorders such as Alzhei

169 heimer disease (AD), the most common form of aging-related neurodegenerative disorders, is associated

170 is also a pathological feature of the major aging-related neurodegenerative disorders.

171 ficient ((-/-)) female mice would have lower aging-related neuroinflammation than wild type (WT).

172 tly affect fatty acid metabolism and augment aging-related neuroinflammation.

173 mechanism for therapeutic intervention into aging-related neuronal disorders.

174 We argue that reversals may not represent aging-related neuronal loss.

175 an important component in the development of aging-related non-melanoma skin cancer.

176 e differences in prevalence and incidence of aging-related outcomes in a rural population (1,358 comm

177 irs the ability of the RPE to defend against aging-related oxidative stress.

178 which represents a viable option to address aging-related pathologies in diabetes and neurodegenerat

179 ent of autophagy may protect against certain aging-related pathologies such as OA.

180 e and genotoxic stresses, protection against aging-related pathologies, and promotion of metabolic ho

181 Aging related phenomena of ooplasmic microtubule dynamic

182 The mechanism behind this aging-related phenomenon is unknown and has been difficu

183 n of Pofut1 in skeletal myofibers can induce aging-related phenotypes in cis within skeletal myofiber

184 t al. (2013) provide a strategy for inducing aging-related phenotypes in hiPSC-derived neurons, enabl

185 1 inhibitor, strikingly ameliorated multiple aging-related phenotypes.

186 The most important aging-related phenotypic effects observed were those tha

187 n regulating mammalian genomic stability and aging-related physiology.

188 ctions and diseases that are enriched in our aging-related predictions and those that are enriched in

189 ence that diseases which are enriched in our aging-related predictions are linked to human aging; and

190 rcc1-deficient liver differs from the normal aging-related process.

191 may indicate a physiological role for NO in aging-related processes.

192 ially in diseases of human aging and in some aging-related processes.

193 In the present study, the effects of AG on aging-related renal and vascular changes and AGE accumul

194 suggest that PPAR-gamma agonists may benefit aging-related renal injury by improving mitochondrial fu

195 noncoding RNAs (ncRNA) also associated with aging-related senescence and cancer, but whether ncRNAs

196 These results show that iNs retain important aging-related signatures, thus allowing modeling of the

197 ermal dysfunction and skin damage as well as aging-related skin diseases, such as epidermal thinning

198 sorder (MDD) have an increased onset risk of aging-related somatic diseases such as heart disease, di

199 tudinal studies, convincing evidence for the aging-related somatic expansion of the C150T mutation, u

200 We propose that AD is initiated by a protein aging-related structural transformation in soluble Abeta

201 r predisposition, atherosclerosis, and other aging related symptoms.

202 ognize and manage multiple comorbidities and aging-related syndromes.

203 isplays multiple phenotypes resembling human aging-related syndromes.

204 The association between aging-related testosterone deficiency and late-onset hyp

205 imilarities of this phenotype to accelerated aging-related thymic involution support the possibility

206 dementia, albeit with increased, presumably aging-related variability, and identify sets of co-expre

207 otype shift to "reactive" ependymal cells in aging-related ventricle stenosis; moreover, they also co

208 baseline total activity score minimized this aging-related weight loss, but this relation was most pr