ライフサイエンスコーパス: normal aging

1 works maintaining cardiac performance during normal aging.

2 the neurophysiology and the neuroanatomy of normal aging.

3 uish the processes of disc degeneration from normal aging.

4 ron populations are reportedly vulnerable to normal aging.

5 underexplored, especially in the context of normal aging.

6 ne in mHR, and thus aerobic capacity, during normal aging.

7 antially preserved numbers of neurons during normal aging.

8 ated aging driven by a DNA repair defect and normal aging.

9 related teaching signals might be altered in normal aging.

10 of factors that influence the trajectory of normal aging.

11 versus frontotemporal lobar degeneration and normal aging.

12 uppresses cellular senescence, and maintains normal aging.

13 ociated with accelerated aging disorders and normal aging.

14 l features associated with schizophrenia and normal aging.

15 med by disease, chemotherapy, radiation, and normal aging.

16 ring those seen much later in life caused by normal aging.

17 n time and support an expectation deficit in normal aging.

18 This phenomenon was previously seen in normal aging.

19 erence on working memory is exacerbated with normal aging.

20 for selective impairment of recollection in normal aging.

21 y to orient attention in time is affected by normal aging.

22 gnitive decline that is commonly observed in normal aging.

23 ification of the processes that occur during normal aging.

24 tcomes and great individual variation during normal aging.

25 ical structural resilience is compromised in normal aging.

26 age range, to document the changes seen with normal aging.

27 aB signaling may contribute to premature and normal aging.

28 orms known to inhibit T cell activation with normal aging.

29 tal or acquired immunodeficiency, and during normal aging.

30 asic mechanisms that may underlie cancer and normal aging.

31 een found to be heritable and to change with normal aging.

32 tanding this syndrome may offer insight into normal aging.

33 which is distinct from that associated with normal aging.

34 go extensive dendritic reorganization during normal aging.

35 ignificantly to cardiomyocyte renewal during normal aging.

36 structural plasticity are maintained during normal aging.

37 al reorganization in the human retina during normal aging.

38 rkinson's, and Huntington's diseases, and in normal aging.

39 intermediate between Alzheimer's disease and normal aging.

40 idence of retinal plasticity associated with normal aging.

41 protection against neuronal cell loss during normal aging.

42 injury, various disease states, disuse, and normal aging.

43 alciumopathy," not merely an acceleration of normal aging.

44 sporadic and familial AD, Down syndrome, and normal aging.

45 two regions that show prominent changes with normal aging.

46 mpaired in myelin-related disorders and upon normal aging.

47 ions of the WRN gene, mimics many changes of normal aging.

48 ers and have been found to accumulate during normal aging.

49 he gray matter volume lost in 10-20 years of normal aging.

50 that are reminiscent of changes seen during normal aging.

51 the overlap of its early-stage markers with normal aging.

52 h may contribute to cognitive decline during normal aging.

53 ce of somatic cells may be a causal agent of normal aging.

54 ochondrial disease and also occur as part of normal aging.

55 rent phases of AD and differentiated AD from normal aging.

56 growth following stress stimulation or with normal aging.

57 e function despite a loss of acinar cells in normal aging.

58 ification which occurs in Fahr's disease and normal aging.

59 e decline in olfactory functions reported in normal aging.

60 r, and pathogen infections as well as during normal aging.

61 proving lifespan and health in both HGPS and normal aging.

62 is, is beneficial for memory function during normal aging.

63 and pathophysiological processes, including normal aging.

64 S1 is crucial for macrophage function during normal aging.

65 d functional connectivity over the course of normal aging.

66 is known about the role of complement during normal aging.

67 licated in many human diseases and occurs in normal aging.

68 t a lack of telomerase accelerates otherwise normal aging.

69 hippocampal pyramidal neuronal function with normal aging.

70 w waves (SWs) change considerably throughout normal aging.

71 load, the presence of metastatic tumors, and normal aging.

72 k factor for neural and cognitive decline in normal aging.

73 nsit--these changes are also observed during normal aging.

74 or recognition memory, which declines during normal aging.

75 viability, regulation of gene expression and normal aging.

76 NS neurodegenerative diseases, as well as in normal aging.

77 upported by the prefrontal cortex decline in normal aging.

78 in conditions including major depression and normal aging.

79 f subclinical disease from changes caused by normal aging.

80 ere highly active in Drosophila brain during normal aging.

81 ry and learning declines are consequences of normal aging.

82 ially in memory, is often viewed as part of "normal" aging.

83 decline in brain function that occurs during normal aging?

84 onclude that beta-MHC gene expression in the normal aging adult and hypertrophic mouse heart is a mar

85 Little is known about how normal aging affects the brain.

86 hese processes, yet we know little about how normal aging affects these early cortical fields.

87 However, normal aging also afflicts prefrontal cortical cognitive

88 These results indicate that normal aging alters teaching signals in the ABL.

89 lved in spatial navigation behaviors and how normal aging alters these network patterns in nonhuman p

90 s considered as a transitional stage between normal aging and a diagnosis of clinically probable Alzh

91 ical studies of the hippocampus/neocortex in normal aging and AD model mice revealed intense calcineu

92 mpairment (aMCI), a transition stage between normal aging and AD.

93 sues, a process that is proposed to underlie normal aging and age-related diseases.

94 ctions play a role in the transition between normal aging and AMD in Bruch's membrane/choroid.

95 ses following an immune challenge occur with normal aging and can elicit or exacerbate neuropathology

96 curs in both chronic heart failure (CHF) and normal aging and contributes to exercise intolerance and

97 uality and activity has been associated with normal aging and correlated with the development of a wi

98 nical condition that is a transition between normal aging and dementia and AD, characterized by a mem

99 Both normal aging and dementia are associated with dysregulat

100 and cerebrospinal fluid [CSF] Abeta1-42 ) in normal aging and dementia in a large multicenter study.

101 Connection of the model to normal aging and disease are discussed.

102 and the APP proteolytic system as a whole in normal aging and disease play.

103 nergetics, i.e., energy metabolism, occur in normal aging and disturbed bioenergetics may be an impor

104 ional state between the cognitive changes of normal aging and early Alzheimer's disease.

105 Molecular and behavioral markers for normal aging and for extended life span in low insulin/I

106 D), and dementia with Lewy bodies (DLB) from normal aging and from each other and the relation of dis

107 vulnerability of hippocampal interneurons to normal aging and highlight that the integrity of a speci

108 f amyloid beta (Abeta) is characteristic for normal aging and human immunodeficiency virus-1 (HIV-1)-

109 ncreased in 4E-BP1 transgenic animals during normal aging and in a response to diet-induced type 2 di

110 Proteasome inhibition occurs during normal aging and in a variety of age-related diseases, w

111 Inhibition of proteasome activity occurs in normal aging and in a wide variety of neurodegenerative

112 o relate changes in tissue structure seen in normal aging and in chronic inflammation to altered lung

113 AGE accumulation, as occurs with normal aging and in disease, may induce receptor-mediate

114 , are the causes of neuronal dysfunctions in normal aging and in early stages of neurodegenerative di

115 C and examined its expression pattern during normal aging and in mice with hypertrophy induced by con

116 ndidate explanation for memory losses during normal aging and indicate that, with regard to plasticit

117 e regional cerebral blood flow (rCBF) during normal aging and investigated its influence on cognitive

118 regional brain iron that is associated with normal aging and is postulated to be exacerbated in neur

119 otease neprilysin (NEP) is down-regulated in normal aging and LOAD.

120 neuronal dysfunction in the context of both normal aging and neurodegenerative conditions, including

121 d in cross-sectional studies is an effect of normal aging and not primarily a birth cohort effect.

122 However, E/A <1.0 is common during normal aging and often is not associated with symptoms o

123 duction of T cells by the thymus accompanies normal aging and parallels the age-dependent increase in

124 pamine function has deteriorated, such as in normal aging and Parkinson's disease.

125 Both normal aging and PFC lesions were associated with decrem

126 r, the cause-and-effect relationship between normal aging and progerin production in normal individua

127 e compared to assess iron homeostasis during normal aging and the effects of increased iron on the fu

128 view the neurophysiology and neuroanatomy of normal aging and the recent recommendations for the clin

129 poiesis-driver mutations (CHDMs) occurs with normal aging and these mutations have been detected in m

130 istinguish between axonal changes created by normal aging and those caused by neurodegenerative disea

131 ective mitophagy is thought to contribute to normal aging and to various neurodegenerative and cardio

132 sight into molecular changes associated with normal aging and will help to better understand the incr

133 e adverse changes formerly considered to be "normal" aging and processes that underlie multiple age-r

134 athology-related tissue characteristics with normal-aging and gender.

135 pression of elt-5 and elt-6 increases during normal aging, and both of these GATA factors repress exp

136 the authors show that noise decreases during normal aging, and provide support for aging-associated i

137 xpression changes with progression of AD and normal aging, and were able to compare functional module

138 nd cognitive functioning that are related to normal aging, and with three measures of overall health.

139 tabolically affected in PET studies of AD or normal aging; and visual cortex, which is relatively spa

140 e findings suggest that Abeta deposition and normal aging are associated with region-specific disrupt

141 pact of changes to protein solubility during normal aging are less well understood.

142 ma and driving neuronal vulnerability during normal aging are unknown.

143 se results suggest that cognitive decline in normal aging arises from functional disruption in the co

144 go moderate neurodegenerative changes during normal aging as well as severe atrophy in Alzheimer's di

145 gy and are often considered to be a part of "normal aging." At the neuronal level, normal aging is kn

146 We found that in normal aging, BC200 levels in cortical areas were reduce

147 important, but that has not been examined in normal aging because of a lack of efficient quantitative

148 also contribute to vascular calcification in normal aging, because progerin progressively accumulates

149 The frequency of MSBs was not altered by normal aging, but decreased by over 50% with surgical me

150 and respiratory chain dysfunction accompany normal aging, but the first direct experimental evidence

151 ecruitment to the CNS is also increased with normal aging, but, to date, no systematic evaluation of

152 uption of the expression of genes related to normal aging by RUNX1 mutations contributes to developme

153 ith AD and those with bvFTD as compared with normal aging by using common T1-weighted structural MR i

154 Normal aging causes a decline in object recognition.

155 Thus, whereas in normal aging cell metabolism is reduced, in the diabetic

156 00 fold, ranging from a 0.5% 5-year risk for normal aging changes to a 50% risk for the highest inter

157 rmed drupelets, should be considered to have normal aging changes with no clinically relevant increas

158 celerated cardiac remodeling associated with normal aging compared with those on a normal diet.

159 In the normal aging cornea, cellular stress has been associated

160 nges that occur in the nervous system during normal aging could provide insight into cognitive declin

161 tipation is not a physiologic consequence of normal aging, decreased mobility, medications, underlyin

162 The experimental results show that for normal aging, education strengthens network reliability,

163 lorectal carcinogenesis, being detectable in normal aging epithelium by using sensitive assays.

164 d hippocampal dysfunction and differentiates normal aging from Alzheimer's disease.

165 Because normal aging has a clear effect on neuroretinal paramete

166 Normal aging has been associated with an increased prope

167 Normal aging has been associated with cognitive changes,

168 Although normal aging has been shown to attenuate Bmal1 expressio

169 in regions are uncertain, and the effects of normal aging have not been examined previously in probab

170 y, and that beta-MHC-expressing cells in the normal aging heart and the hypertrophic heart are distri

171 role of dysregulated epigenetic modifiers in normal aging hematopoiesis, which may include support to

172 in many disease conditions as well as during normal aging; however, small-molecule agents that reduce

173 enase-hyperreactive (COX-/SDH++) fibers from normal aging human subjects and identified mtDNA-deletio

174 Whereas normal aging impairs specific aspects of language produc

175 Normal aging in both rodents and humans is often charact

176 xonal layer was significantly increased with normal aging in control (CNT) mice (p < 0.01) but remain

177 auditory brain processing that accompanying normal aging in humans, preserving robust speech recogni

178 ly distinguish Alzheimer's disease (AD) from normal aging in individual scans.

179 We speculate that declining APP during normal aging in males may contribute to the loss of sexu

180 rker of pathological cardiac hypertrophy and normal aging in many experimental models.

181 nctional connectivity, Abeta deposition, and normal aging in mouse models.

182 defined patterns of tau tracer retention in normal aging in relation to age, cognition, and beta-amy

183 To investigate the loss of neurons with normal aging in rodents, we used unbiased stereological

184 ccommodation, is altered during learning and normal aging in the brain.

185 reatments to ameliorate cognitive decline in normal aging in the future.

186 y is transcriptionally down-regulated during normal aging in the human brain.

187 nificantly enhanced neuroinflammation during normal aging in WT mice and in response to AD-associated

188 en correlated with neurological diseases and normal aging; in particular, in area 46 of the rhesus mo

189 the loss of muscle mass and strength during normal aging, involves coordinate changes in skeletal my

190 This implies that a major effect of normal aging is a degradation of the hierarchical proces

191 We show that normal aging is accompanied by a profound loss of histon

192 Normal aging is accompanied by changes in hypothalamic f

193 Here we explore the possibility that normal aging is accompanied by disruptive alterations in

194 Normal aging is associated with a decline in episodic me

195 Furthermore, normal aging is associated with a decline in sensory, mo

196 Normal aging is associated with a variable decline in co

197 Here, we use fMRI to show that normal aging is associated with diminished selectivity o

198 Normal aging is associated with impairments in stimulus

199 Normal aging is associated with precipitous drops in cog

200 Normal aging is associated with progressive functional l

201 rt of "normal aging." At the neuronal level, normal aging is known to be associated with numerous cel

202 Normal aging is often accompanied by impairments in form

203 Normal aging is often associated with a decline in learn

204 Normal aging is often difficult to distinguish from the

205 ppocampal cortistatin mRNA expression during normal aging is significantly attenuated in Tg mice at a

206 Whether lamin A plays any role in normal aging is unknown.

207 Normal aging is usually accompanied by increased difficu

208 A central problem in the neurobiology of normal aging is why learning is preserved in some aged i

209 n of mitochondrial DNA mutations accelerates normal aging, leads to oxidative damage to nuclear DNA,

210 aberrant methylation is commonly present in normal aging livers, and sequentially progresses with ad

211 hat abnormal regulation of the mechanisms of normal aging may contribute to the pathobiology of both

212 ts, as the cognitive changes associated with normal aging may have an adverse impact on decision-maki

213 Alzheimer's disease and normal aging may impair retrograde transport of nerve gr

214 tations occurring in dopamine neurons during normal aging may predispose individuals to the developme

215 During normal aging, men experience a significant decline in te

216 nit c accumulation in autophagic vacuoles in normal aging mice.

217 ty in 52 individuals across the continuum of normal aging, mild cognitive impairment (MCI), and mild

218 cceleration of some symptoms associated with normal aging, most notably cardiovascular disease that e

219 protein levels dramatically increase in the normal aging mouse and human brain, by as much as 300-fo

220 at Sod1(-/-) mice display characteristics of normal aging muscle in an accelerated manner and propose

221 ect with no apparent retinal aging (n = 15), normal aging (n = 15), early AMD (n = 15), and intermedi

222 ral lobar degeneration (N = 11 patients) and normal aging (N = 24 subjects).

223 erous behavioral studies have suggested that normal aging negatively affects source memory accuracy f

224 are especially vulnerable to the effects of normal aging, neurological disease or disruption of sens

225 This study provides further evidence that in normal aging neurons are not lost and hence cannot accou

226 non-HGPS individuals, and most hallmarks of normal aging occur in progeria, research on HGPS can ide

227 mine whether hepatic changes that occur with normal aging occur prematurely in Ercc1(-/Delta) mice, w

228 We observe noise reduction during normal aging of a cell, followed by a short catastrophe

229 GSIS increases during the normal aging of mice and is driven by elevated p16(Ink4a

230 Nevertheless, a role for cytokines in normal aging of the human brain has not been confirmed,

231 It is challenging to separate the effects of normal aging of the retina and visual pathways independe

232 input fails to account for the influence of normal aging on memory supported by the primate hippocam

233 help gain better insight into the effects of normal aging on the neurons and neuroglial cells in the

234 In this study, we assess the impact of normal aging on top-down modulation, a cognitive control

235 tically determine their effects, or those of normal aging, on brain structure in vivo.

236 of the decline of visual sensitivity due to normal aging or age-related eye diseases, thus potential

237 confers major risk for impaired cognition in normal aging or Alzheimer's disease (AD).

238 yes in which POAG did not develop represents normal aging or glaucomatous change not detected by conv

239 Nephron loss due to normal aging or renal surgery (CKD-S) may have lower lik

240 d was insensitive to changes associated with normal aging or to slight variations in cartilage thickn

241 As the cortex thins with normal aging, our data suggest that smoking is associate

242 steeper decreases of hippocampal volume with normal aging (p = 0.026).

243 ve been associated with various diseases and normal aging, particularly in tissues with high energy d

244 hite matter border on MRI is associated with normal aging, pathological aging, and the presence of fo

245 FR at a higher rate than what is seen in the normal aging population.

246 teroidal anti-inflammatory drugs (NSAIDs) in normal aging populations reduces the risk of developing

247 We demonstrate that, as in humans, normal aging primarily manifests as defects in relaxatio

248 Normal aging primes, or sensitizes, microglia, and this

249 ur in a subpopulation of tissue cells during normal aging, probably predisposing them for tumorigenes

250 conditions offer valuable insights into the normal aging process and the complex biology of cardiova

251 d altered NAD homeostasis that accompany the normal aging process but also, elucidate the merits and

252 eases that resemble premature aging--and the normal aging process has been a source of debate in the

253 ne 125 phosphorylation diminished during the normal aging process in both humans and flies.

254 se in brown fat activity observed during the normal aging process is currently unknown.

255 r changes of nuclear architecture during the normal aging process of a multicellular organism, but al

256 n that myelin abnormalities characterize the normal aging process of the brain and that an age-associ

257 ynamic nature of the CSF proteome during the normal aging process.

258 ght into how progerin may participate in the normal aging process.

259 50 as causing similar mitotic defects in the normal aging process.

260 PS is likely a result of acceleration of the normal aging process.

261 ges in nuclear architecture occur during the normal aging process.

262 People develop presbyopia as part of the normal aging process.

263 Changes in sleep pattern are typical for the normal aging process.

264 ive oxygen species, are both associated with normal aging processes and linked to cardiovascular dise

265 anisms have identified major roadblocks that normal aging processes impose on tissue regeneration.

266 ffort to explain how protein aggregation and normal aging processes might be involved in polyglutamin

267 suggest that elevated Pdyn expression during normal aging reduces mGluR expression and signaling, whi

268 dy in Ercc1-deficient liver differs from the normal aging-related process.

269 isms that maintain neuronal integrity during normal aging remain elusive.

270 progenitor cell dysfunction and depletion in normal aging remains incompletely understood.

271 high level of specificity by accounting for normal aging (requiring a significant negative slope tha

272 In both structures, normal aging results in a 20% decrease in the number of

273 Normal aging results in a progressive loss of SIRT1 in w

274 e of neurodegeneration and cell death in the normal aging rhesus monkey.

275 or understanding the inflammatory changes in normal aging skin.

276 Yet in normal aging, studies indicate that neurons are not lost

277 pothesized to underlie cognitive deficits in normal aging subjects, but the mechanisms that underlie

278 Although characterized by features of normal aging such as alopecia, skin wrinkling, and osteo

279 nt changes associated with the physiology of normal aging that can significantly influence this proce

280 In contrast to normal aging, the presence of amyloid increased apoE3, w

281 About half of these genes also affected normal aging, thereby linking these two processes mechan

282 heat shock protein expression increased with normal aging, this process was accelerated in rTg4510 mi

283 1 x 10-26) and longitudinal progression from normal aging to AD (NIA ADC, Cochran-Armitage trend test

284 subjects with cognitive states ranging from normal aging to AD-including mild cognitive impairment (

285 wn of brain networks during progression from normal aging to Alzheimer disease dementia (AD) has also

286 F1, links maintenance of telomere length and normal aging to attenuation of inflammatory cytokine exp

287 isintegration of the intrinsic networks from normal aging to MCI to AD was inversely proportional to

288 During normal aging up to one year, the percentage of GFP+ card

289 roughout adulthood increases survival during normal aging (up to 46% median increase).

290 ween gene expression changes associated with normal aging vs. memory performance.

291 Normal aging was associated with reduced bilateral funct

292 Region-specific mtDNA damage with normal aging was evaluated in 45 control subjects (ages

293 Strikingly, in contrast to normal aging, we observe transcriptional up-regulation o

294 ere is a loss of dopamine neurons as part of normal aging, we show this very effect.

295 stemic chronic inflammation, observed during normal aging, were prevented.

296 This protein is reduced over the course of normal aging, which is a major risk factor for Parkinson

297 tissue in the arcuate fasciculus occurs with normal aging, while having limited impact on tract organ

298 These finding on normal aging will provide a reference for comparing pote

299 tion of the normal-appearing white matter in normal aging, with relative sparing of sensorimotor fibe

300 rhesus monkey provides an excellent model of normal aging without the potential confounds of incipien