ライフサイエンスコーパス: normal aging

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

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

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

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

5 or recognition memory, which declines during normal aging.

6 viability, regulation of gene expression and normal aging.

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

8 upported by the prefrontal cortex decline in normal aging.

9 in conditions including major depression and normal aging.

10 f subclinical disease from changes caused by normal aging.

11 ere highly active in Drosophila brain during normal aging.

12 ry and learning declines are consequences of normal aging.

13 the neurophysiology and the neuroanatomy of normal aging.

14 uish the processes of disc degeneration from normal aging.

15 ron populations are reportedly vulnerable to normal aging.

16 underexplored, especially in the context of normal aging.

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

18 antially preserved numbers of neurons during normal aging.

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

20 related teaching signals might be altered in normal aging.

21 of factors that influence the trajectory of normal aging.

22 versus frontotemporal lobar degeneration and normal aging.

23 uppresses cellular senescence, and maintains normal aging.

24 ociated with accelerated aging disorders and normal aging.

25 l features associated with schizophrenia and normal aging.

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

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

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

29 This phenomenon was previously seen in normal aging.

30 erence on working memory is exacerbated with normal aging.

31 for selective impairment of recollection in normal aging.

32 rotein aggregation has been described during normal aging.

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

34 gnitive decline that is commonly observed in normal aging.

35 ification of the processes that occur during normal aging.

36 tcomes and great individual variation during normal aging.

37 ical structural resilience is compromised in normal aging.

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

39 aB signaling may contribute to premature and normal aging.

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

41 order MDD, BD, SZ, AD, and PD, as well as in normal aging.

42 tal or acquired immunodeficiency, and during normal aging.

43 asic mechanisms that may underlie cancer and normal aging.

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

45 aging may lead to a better understanding of normal aging.

46 tanding this syndrome may offer insight into normal aging.

47 go extensive dendritic reorganization during normal aging.

48 ignificantly to cardiomyocyte renewal during normal aging.

49 structural plasticity are maintained during normal aging.

50 al reorganization in the human retina during normal aging.

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

52 intermediate between Alzheimer's disease and normal aging.

53 idence of retinal plasticity associated with normal aging.

54 protection against neuronal cell loss during normal aging.

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

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

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

58 two regions that show prominent changes with normal aging.

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

60 disease, traumatic brain injury, and even in normal aging.

61 o significant structural rearrangements with normal aging.

62 n neurogenesis and cognitive function during normal aging.

63 works maintaining cardiac performance during normal aging.

64 which is distinct from that associated with normal aging.

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

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

67 e decline in olfactory functions reported in normal aging.

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

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

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

71 and pathophysiological processes, including normal aging.

72 S1 is crucial for macrophage function during normal aging.

73 d functional connectivity over the course of normal aging.

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

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

76 t a lack of telomerase accelerates otherwise normal aging.

77 hippocampal pyramidal neuronal function with normal aging.

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

79 decline in brain function that occurs during normal aging?

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

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

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

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

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

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

86 provide clarification of differences between normal aging and AD, and elucidate the transition betwee

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

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

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

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

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

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

93 me degree of astrogliosis is associated with normal aging and degenerative conditions such as Alzheim

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

95 Both normal aging and dementia are associated with dysregulat

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

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

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

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

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

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

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

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

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

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

106 lators of the aging process, decrease during normal aging and in aging-related diseases.

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

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

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

110 evident in more effortful cognitive tasks in normal aging and in those suffering dopamine-dependent n

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

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

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

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

115 sleep/wake architecture are also present in normal aging and may represent a significant risk factor

116 ociated with memory and cognitive decline in normal aging and mild cognitive impairment remains elusi

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

118 overt neuronal death is a shared feature of normal aging and neurodegenerative disorders, but the in

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

120 Both normal aging and PFC lesions were associated with decrem

121 athies with prospective cognitive decline in normal aging and preclinical Alzheimer's disease (AD) re

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

123 ion of tau and Abeta may affect cognition in normal aging and the asymptomatic stage of AD.

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

125 aging brain and reveal relationships between normal aging and the evolution of AD.

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

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

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

129 CAA occurs with normal aging and to various degrees in AD, where its imp

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

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

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

133 ons (streptozotocin-induced diabetes, during normal aging, and after unilateral ureteral obstruction)

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

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

136 he anterolateral entorhinal cortex (EC) with normal aging, and that the presence of beta-amyloid (Abe

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 ostasis and lead to symptoms associated with normal aging as well as dementia.

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

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

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

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

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

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

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

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

153 Normal aging causes a decline in object recognition.

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

155 00 fold, ranging from a 0.5% 5-year risk for normal aging changes to a 50% risk for the highest inter

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

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

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

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

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

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

162 Because normal aging has a clear effect on neuroretinal paramete

163 Normal aging has been associated with an increased prope

164 Normal aging has been associated with cognitive changes,

165 Although normal aging has been shown to attenuate Bmal1 expressio

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

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

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

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

170 ined the cochlear sensory epithelium from 23 normal-aging humans (14 males and 9 females), 0-86 years

171 Whereas normal aging impairs specific aspects of language produc

172 Normal aging in both rodents and humans is often charact

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

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

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

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

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

178 lar dendritic spine loss to that observed in normal aging in monkeys, but so far without detection of

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

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

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

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

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

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

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

186 Normal aging, in the absence of dementia, also results i

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

188 g in multiple sclerosis (MS) attributable to normal aging increased from 42.7% and 16.7% respectively

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 accompanied by escalating systemic infla

195 Normal aging is associated with a decline in episodic me

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

197 Normal aging is associated with a variable decline in co

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

199 Normal aging is associated with impairments in stimulus

200 Normal aging is associated with precipitous drops in cog

201 Normal aging is associated with progressive functional l

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 However, the neurologic role of TREM2 in normal aging is poorly understood.

206 aping neuronal and cognitive function during normal aging is underexplored.

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

208 Normal aging is usually accompanied by increased difficu

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

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

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

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

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

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

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

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

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

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

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

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

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

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

223 CpH methylation losses occur in normal aging neurons, but are accelerated in AD.

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

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

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

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

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

229 neural white matter changes as a function of normal aging on action selection performance.

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

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

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

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

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

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

236 her retinal atrophy persists in PMS, exceeds normal aging, or can be distinguished from relapsing-rem

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

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

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

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

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

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

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

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

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

246 chers because of its involvement in both the normal aging process and common human diseases.

247 Furthermore, we show that the normal aging process and Sotos syndrome share methylatio

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

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

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

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

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

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

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

255 n health through a range of diseases and the normal aging process.

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

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

258 50 as causing similar mitotic defects in the normal aging process.

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

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

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

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

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

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

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

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

267 tion selection and how these are affected by normal aging remain to be elucidated.

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

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

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

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

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

273 or understanding the inflammatory changes in normal aging skin.

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

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

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

277 In normal aging, the balance between bone resorption and fo

278 In normal aging, the FD% increased with age across the cent

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

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

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

282 1 x 10-26) and longitudinal progression from normal aging to AD (NIA ADC, Cochran-Armitage trend test

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

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

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

286 reduced along with disease progression from normal aging to early AD, and cerebrospinal fluid (CSF)

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 widely across individuals, especially during normal aging, with impaired sleep contributing to defici

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

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