ライフサイエンスコーパス: aged mice

1 s: 4-5 months (young mice) and 12-13 months (aged mice).

2 negative isolation membranes in neurons from aged mice.

3 0 signaling led to B-cell lymphomagenesis in aged mice.

4 restoring delayed macrophage recruitment in aged mice.

5 ell deletion rejuvenates pulmonary health in aged mice.

6 ppocampus and improves cognitive function in aged mice.

7 ion loss in a mouse model of glaucoma and in aged mice.

8 re HSC function and the immune repertoire in aged mice.

9 se results in transgenic, non-transgenic and aged mice.

10 n both fast aging Xpd(TTD/TTD) and naturally aged mice.

11 endent "context discrimination (CS) test" in aged mice.

12 icity and hippocampal-dependent cognition in aged mice.

13 g autophagy and improving vessel function in aged mice.

14 ere evident when the mutation was induced in aged mice.

15 revented by long-term caloric restriction in aged mice.

16 ssociated metabolic disorders in fat-fed and aged mice.

17 D31(hi)Emcn(hi) vessel and bone formation in aged mice.

18 es of BACE1, causes reduced spine density in aged mice.

19 hroughput RNA-Sequencing of kidney tissue in aged mice.

20 SNHL by impairing cochlear myelination in WT aged mice.

21 rarily restored normal sequence structure in aged mice.

22 een neuroinflammation and hypermetabolism in aged mice.

23 -renewal and restored immune cell content in aged mice.

24 ot only in the skin but also in the serum of aged mice.

25 cline of the affected SVZ-stem cell niche in aged mice.

26 jury and restored endogenous HSC function in aged mice.

27 tions to voluntary wheel running in young or aged mice.

28 re naive T cell homeostatic proliferation in aged mice.

29 +) dynamics in eggs from young and naturally-aged mice.

30 uvenated the aged HSCs and MuSCs in normally aged mice.

31 tiated after stroke, would delay recovery in aged mice.

32 ted with the extent of cognitive deficits in aged mice.

33 slow gamma activity but not SWR abundance in aged mice.

34 as determined by Morris water maze (MWM), in aged mice.

35 binol rescued the barrier deficiency even in aged mice.

36 chanism of active zone proteins in NMJs from aged mice.

37 and improve measures of healthspan in middle-aged mice.

38 associated with declining levels of IL-2 in aged mice.

39 a-cell mass, leading to islet hyperplasia in aged mice.

40 impaired dopamine homeostasis and release in aged mice.

41 nd decreased bone marrow fat accumulation in aged mice.

42 investigated the origin of CD25(lo) Tregs in aged mice.

43 MI checkpoint is compromised in oocytes from aged mice.

44 ion studies show altered dopamine release in aged mice.

45 Tregs, naive T cells, and memory T cells in aged mice.

46 gnitive decline and enhances neurogenesis in aged mice.

47 ted to increase the generation of neurons in aged mice.

48 icity and overall behavioral capabilities of aged mice.

49 nt-binding protein (CREB)-regulated genes in aged mice.

50 tional defect in fine odor discrimination in aged mice.

51 brain and enhanced the cognitive function of aged mice.

52 well as strengthening of damaged muscles of aged mice.

53 first 24 weeks of adult life but depleted in aged mice.

54 ranscriptional changes in the hippocampus of aged mice.

55 rulonephritis and a range of malignancies in aged mice.

56 acetylation at the c-fos promoter region in aged mice.

57 d neuron formation and olfactory function in aged mice.

58 , after fear conditioning were diminished in aged mice.

59 ted fibrosis, was observed in both adult and aged mice.

60 evels were diminished in CD8(+) T cells from aged mice.

61 ed effector CD8+ T cell polyfunctionality in aged mice.

62 ein kinase signaling in satellite cells from aged mice.

63 rkers of the effects of haloperidol (HAL) in aged mice.

64 not preserve its IgM germline status in the aged mice.

65 is factor alpha in skin and heart tissues of aged mice.

66 exacerbations of dry eye disease observed in aged mice.

67 dult neurogenesis and cognition to sedentary aged mice.

68 tered between Ctrl and AD mice and naturally aged mice.

69 hat this circulating factor is attenuated in aged mice.

70 memory deficits were also seen in naturally aged mice.

71 ting components was distinct in young versus aged mice.

72 and continued to drop to very low levels in aged mice.

73 ignificantly improves learning and memory in aged mice.

74 results in a beneficial metabolic effect in aged mice.

75 evelopment and affects lipoprotein levels in aged mice.

76 p53 in beiging WAT of young mice but not in aged mice.

77 s after stroke in male and female, young and aged mice.

78 a novel GRA (JNJ-46207382) to both young and aged mice.

79 al defects in autophagosomes in neurons from aged mice.

80 ity and cognitive deficits, in the brains of aged mice.

81 nal state and improves cognitive function in aged mice.

82 ylation ameliorates cognitive impairments in aged mice.

83 l and delays skeletal muscle degeneration in aged mice.

84 ng-lasting neuropathological effects also in aged mice (10 months), such as reduced volumes of cerebe

85 Here, we show that aged mice (18-19 months) had reduced functional recovery

86 Young mice (2 to 3 months old) and aged mice (22 to 28 months old) were rendered susceptibl

87 In the current study, aged mice (22-25 months old) exhibited significantly inc

88 n, astrocytic Apoe dramatically decreased in aged mice, a decrease that was prevented by exercise.

89 In aged mice, a single injection of HT-0712 significantly b

90 Conversely, loss of FGF21 function in middle-aged mice accelerated thymic aging, increased lethality,

91 In aged mice, accumulation of RanGAP1 together with polyglu

92 lts, young C57BL/6 mice (age 3-4 mo), middle-aged mice (age 10-12 mo), and aged mice (age 24-26 mo) w

93 -4 mo), middle-aged mice (age 10-12 mo), and aged mice (age 24-26 mo) were subjected to left anterior

94 neurons, effects that were also observed in aged mice, albeit to a lesser extent, indicating preserv

95 The aged mice also had a significant increase in F4/80(+) he

96 Increased GDF11 levels in aged mice also improved muscle structural and functional

97 inistration of recombinant GDF11 (rGDF11) to aged mice alters aging phenotypes in the brain, skeletal

98 a-cell proliferation was severely reduced in aged mice, although still present at 3.2-fold the very l

99 creasing systemic concentrations of Gpld1 in aged mice ameliorated age-related regenerative and cogni

100 by faecal transfers from younger adults into aged mice and by immunisations with cholera toxin, witho

101 from ABSCs emerged exclusively in the ICZ of aged mice and contributed to airway homeostasis and repa

102 did not differ with laser-injury in young or aged mice and did not significantly change in the periph

103 ctor CD8+ T cell apoptosis in both young and aged mice and enhanced effector CD8+ T cell polyfunction

104 ce the functions of stem/progenitor cells in aged mice and extend lifespan.

105 rses long-term memory (LTM) deficits in both aged mice and flies.

106 ed 7KCh and microglia to the outer retina of aged mice and investigated 7KCh effects on retinal micro

107 determined that NETosis is more prevalent in aged mice and investigated the role of PAD4/NETs in age-

108 minished in uterine (and tail) arteries from aged mice and post-menopausal women.

109 duced beta-cell proliferation in islets from aged mice and protected from hyperglycemia-induced endop

110 ignificantly improves learning and memory in aged mice and reduces 5hmC abundance in mouse hippocampu

111 ) signaling contributed to muscle atrophy in aged mice and results from 15-PGDH-expressing myofibers

112 increase in severe hyperlipidemic blood from aged mice and upon feeding a high-fat diet (Apoe(-/-) mi

113 nd it is increased within the hippocampus of aged mice and young heterochronic parabionts.

114 ystemic challenge relative to Prevnar-immune aged mice and young mice that had received either vaccin

115 orrelate with improved cognitive function in aged mice, and concentrations of Gpld1 in blood were inc

116 SARS-CoV-2 MA caused more severe disease in aged mice, and exhibited more clinically relevant phenot

117 recision and neuronal IL-33 are decreased in aged mice, and IL-33 gain of function mitigates age-rela

118 ased levels of H3K9me3 in the hippocampus of aged mice, and improved performance in the objection loc

119 ision rates did not decrease in the colon of aged mice, and only small decreases were observed in the

120 Cultured senescent tubular cells, kidneys of aged mice, and renal stress models exhibited upregulatio

121 n the SR as prominent target of glycation in aged mice, and the sites of glycation were characterized

122 ainst C. difficile toxin A were depressed in aged mice, and vancomycin treatment reduced antibody res

123 Blood flow and angiogenesis in aged mice are also enhanced on administration of bisphos

124 Two-thirds of MuSCs from aged mice are intrinsically defective relative to MuSCs

125 the H chain (V(H)) use in both the young and aged mice as compared with peritoneal PtC(+) B-1a cells.

126 Aged mice as well as mice with reduced DC function had d

127 phenotypes of bone marrow MSCs derived from aged mice, as well as promoting their proliferation, col

128 ost MHC genes remained more downregulated in aged mice at day 3.

129 ration of alphaKG increases the bone mass of aged mice, attenuates age-related bone loss, and acceler

130 thway is strongly de-regulated in MuSCs from aged mice because of insufficient attachment to the nich

131 ICOS contributed to Treg maintenance in aged mice, because in vivo Ab blockade of ICOSL led to a

132 Surprisingly, aged mice but not mice with genetically altered DC funct

133 reased the levels of Parkin in the aortas of aged mice but not young mice.

134 regulatory T cell accumulation in naturally aged mice, but not inflammatory infiltration.

135 Lastly, inoculation of alpha-Syn fibrils in aged mice, but not younger mice, resulted in progression

136 Tfh and cDC2 cell response can be boosted in aged mice by treatment with a TLR7 agonist.

137 of meningeal lymphatic drainage function in aged mice can ameliorate TBI-induced gliosis.

138 The changes in synaptic transmission in aged mice can be partially rescued by improving calcium

139 rminal centre reaction in Peyer's patches of aged mice can be rescued by faecal transfers from younge

140 suggesting that the poor stroke recovery in aged mice can be reversed via poststroke bacteriotherapy

141 s to IL-10 production from CD4(+) T cells in aged mice, causing attenuated responses of CD8(+) T cell

142 ctive in young mice and greatly inhibited in aged mice, coinciding with spatial memory deficits.

143 d, and recovery from infection was slower in aged mice compared to young mice.

144 f activity onset and acrophase is delayed in aged mice compared to younger mice.

145 d in LACC1 KO mice undergoing CIA as well as aged mice compared with WT controls.

146 e record a 36% decrease in BCSFB function in aged mice, compared to a 13% decrease in parenchymal blo

147 Brain samples from aged mice contain G4-DNA structures that are absent in b

148 Calorie-restricted aged mice contain less visceral fat and displayed reduce

149 revious studies have shown B-1a cell Ig from aged mice contains abundant nontemplated (N)-additions.

150 Neonatal B1 B cells and their CLL progeny in aged mice continued to express moderately up-regulated c

151 nescent beta-catenin-depleted hepatocytes in aged mice create an inflammatory microenvironment that s

152 Aged mice deficient in microRNA (miRNA/miR)-146a succumb

153 enhanced contextual fear memory in adult and aged mice demonstrating improved hippocampal function.

154 In addition to neurodegeneration, aged mice developed a degenerative myopathy, with scatte

155 Nonetheless, Pneumovax-immunized aged mice developed limited bacteremia following respira

156 on secondary exposure to desiccating stress, aged mice developed more severe corneal epitheliopathy t

157 p defective long-term potentiation (LTP) and aged mice display spatial learning and memory deficits t

158 Aged mice displayed a CA1 long-term potentiation (LTP) d

159 nhibition of LTbetaR signalling in young and aged mice disrupted smoking-related inducible bronchus-a

160 ally improved the survival outcome of middle-aged mice during both polymicrobial sepsis and sterile e

161 s lack of intestinal granulocyte response in aged mice during severe C. difficile infection was accom

162 lations that produce interleukin-6 in middle-aged mice during systemic inflammation.

163 to either sublethally irradiated or normally aged mice effectively depleted SCs, including senescent

164 PERK expression in the hippocampus of middle-aged mice enhances hippocampal-dependent learning and me

165 young mice sleep less than do middle-aged or aged mice, especially during the night, while the timing

166 ox-modified disease networks that remodel in aged mice, establishing a systemic molecular basis for t

167 deletion in young high-fat diet fed mice or aged mice exacerbated glucose intolerance with inadequat

168 Here we demonstrated that aged mice exhibit poor effector CD8+ T cell polyfunction

169 animals during infection, but TFH cells from aged mice exhibit significant differences, including red

170 ed largely on studies showing that HSCs from aged mice exhibit these lineage biases following transpl

171 Aged mice exhibited reduced pulmonary immune profiles an

172 ution and morphology of retinal terminals in aged mice exhibiting varying levels of axonal transport

173 wed that a majority of accumulating Tregs in aged mice expressed low levels of CD25, and their accrua

174 observed within a subset of astrocytes, and aged mice expressing PDGFRbeta(D849V) exhibited reactive

175 Moreover, in the aged mice, expression levels of several genes whose expr

176 HSCs from aged mice fail to down-regulate Rad21/cohesin and inflam

177 Although eggs from aged mice feature a reduced ability to replenish intrace

178 significantly improved glucose tolerance in aged mice fed a chow (~30% vs. saline) or HF (~50% vs. s

179 Aged mice fed a control diet were exquisitely more susce

180 nistered rGDF11 or rGDF8 protein to young or aged mice fed a standard chow diet, short-term high-fat

181 ntly improves metabolic fitness in naturally aged mice fed with a regular diet (RD).

182 ting cell frequencies were 10-fold higher in aged mice following Pneumovax immunization relative to y

183 The administration of JAK inhibitor to aged mice for 10 wk alleviated both adipose tissue and s

184 tion of apoE4 in astrocytes does not protect aged mice from apoE4-induced GABAergic interneuron loss

185 t, deletion of apoE4 in neurons does protect aged mice from both deficits.

186 separates satellite cell gene expression in aged mice from that in young mice.

187 mics of NG2(+) glial cells in the mature and aged mice gray matter.

188 ondrial function in the pancreatic islets of aged mice (>/=24 months), the result of 52% and 57% defe

189 skin and serum increase in otherwise normal, aged mice (>12 months).

190 Aged mice had a relative inability to upregulate gene ex

191 and Enterobacteriaceae were mostly similar, aged mice had a significant change in the Firmicutes to

192 iN cells from aged mice had apparently normal active and passive neuro

193 d mediator metabololipidomics, we found that aged mice had both delayed resolution and reduced SPMs.

194 use model of RSV pathogenesis, we found that aged mice had impaired Ag-specific CD8(+) T cell respons

195 -directly exposed to SR calcium release-from aged mice had increased calcium content compared with th

196 polymicrobial sepsis, and subsequently, the aged mice had increased mortality and defective peritone

197 Importantly, in aged mice harboring a genetic burden relevant for human

198 Also, more influenza specific T cells in aged mice have a regulatory phenotype, which could contr

199 Here, we demonstrate that older people and aged mice have impaired Tfh cell differentiation upon va

200 Here, we find that MII oocytes from aged mice have less securin than oocytes from young mice

201 TPN2 deficiency prevented tumours forming in aged mice heterozygous for the tumour suppressor p53.

202 pithelium of multiple middle-aged versus old-aged mice highlighted the consistent up-regulation of th

203 Reprogramming of fibroblasts from adult and aged mice, however, has not yet been explored in detail.

204 and improves cognitive function in adult and aged mice; however, whether neuronal Cav-1 overexpressio

205 This study in juvenile-adolescent aged mice identifies a novel form of synaptic plasticity

206 ic administration of young blood plasma into aged mice improved age-related cognitive impairments in

207 gnaling, and that antagonism of miR-19a/b in aged mice improves blood flow recovery after ischemia an

208 restored protein solubility in the lenses of aged mice in vivo and in human lenses ex vivo.

209 s, suppresses characteristic PD hallmarks in aged mice, including SNc DA neuron loss, motor deficits,

210 In aged mice, increased voiding frequency and enhanced low

211 Finally, in aged mice, increasing cellular excitability and activati

212 llowing lysolecithin demyelination in middle-aged mice, indapamide treatment was associated with decr

213 In aged mice, inducible p53 ablation in differentiated adip

214 Aged mice injected intratracheally with TNF-alpha exhibi

215 ments indicate that impaired regeneration in aged mice is reversible by exposure to a young circulati

216 Notably, increased white matter repair in aged mice is translated into significant poststroke moto

217 stics under stressed conditions in young and aged mice is unknown.

218 Moreover, aged mice lacking Tec kinase developed a mild autoimmune

219 fter initial exposure to desiccating stress, aged mice maintained higher frequencies of memory Th17 c

220 Thus, reduced bacterial diversity in aged mice may contribute to increased P. gingivalis colo

221 st that reduced DC numbers in lymph nodes of aged mice may involve the effect of advanced glycation e

222 In aged mice, novel nano-proresolving medicines carrying as

223 rsus control (CTL) mice, basally in young or aged mice, or even when hearts were subjected to hemodyn

224 that Sirt1 activators increase bone mass in aged mice, our results also suggest that Sirt1 could be

225 rity of murine trauma and shock in young and aged mice over time, and by examining the response in is

226 Excitingly, in aged mice overexpressing neuronal OGT in the aged hippoc

227 We found that, after extended training, aged mice produced shorter actions and displayed squeeze

228 ment of bone marrow-derived macrophages from aged mice protected cells form a pro-inflammatory phenot

229 Treatment of diabetic and aged mice recruits fibroblasts to the wound bed and redu

230 or extracellular matrix content in young or aged mice, regardless of running activity.

231 systemic administration of young plasma into aged mice rejuvenates memory in an autophagy-dependent m

232 the residual functional MuSC population from aged mice, rejuvenating its potential for regeneration a

233 obulin G (IgG) levels in Pneumovax-immunized aged mice relative to other groups.

234 Unexpectedly, we find that aged mice remain behaviorally circadian and that their e

235 Strikingly, alpha-Toc supplementation of aged mice resulted in a 1000-fold lower bacterial lung b

236 fully promote an IL-4/IL-4Ralpha response in aged mice resulted in attenuated arginase (M2a associate

237 endent, spontaneous inflammasome activity in aged mice resulted in impaired glucose tolerance that co

238 atin marks in activated satellite cells from aged mice, resulting in the specific induction of Hoxa9

239 on of FOXN1 in the fully involuted thymus of aged mice results in robust thymus regeneration characte

240 led histologic and ultrastructural assays of aged mice revealed that post-mitotic hippocampal pyramid

241 Depletion experiments in aged mice revealed TIMP2 to be necessary for the cogniti

242 t introduction of blood from young mice into aged mice reversed age-associated cognitive impairments

243 trikingly, most haematopoietic stem cells in aged mice share these altered metabolic and functional f

244 Notably, SCs in aged mice show altered beta1-integrin activity and insen

245 However, aged mice show an increase in the amount of sleep, where

246 creased with advancing age, such that middle-aged mice showed much more pronounced differences compar

247 ecific c-Kit overexpression (c-KitbetaTg) in aged mice showed significantly increased islet vasculatu

248 Aged mice showed significantly poorer contextual and tra

249 gly, introducing just the activated APC into aged mice significantly enhances otherwise compromised A

250 In aged mice, skeletal blood flow and endothelial Notch act

251 mented lung injury to the levels observed in aged mice stimulated with TNF-alpha alone.

252 At 2 d postinfection, aged mice suffered 1000-fold higher pulmonary bacterial

253 pS214-Tau was not observed in normal aged mice, suggesting that it arises with the evolutiona

254 d self-renewal of NPCs were also impaired in aged mice, suggesting that the down-regulation of protea

255 after satellite cell depletion in young and aged mice suggests that Pax3+ cells may compensate for a

256 Here, we demonstrate in aged mice that spontaneously elevated TNF represents a c

257 and lifespan extension were achieved in mid-aged mice that were locally implanted with healthy hypot

258 thin demyelination model in young and middle-aged mice, the latter group developed greater acute axon

259 t the high inflammatory response observed in aged mice, the sequential delivery of MCP-1/IL-4 was cap

260 In aged mice, this response was induced by brain-derived si

261 tigen-specific immune responses in young and aged mice through the upregulation of immunomodulatory g

262 uggest that alpha-Toc enhances resistance of aged mice to bacterial pneumonia by modulating the innat

263 e, rats and nonhuman primates [NHPs]) and in aged mice to examine the effects of the selective M(1) P

264 y decreased the enlarged memory Th17 pool in aged mice to frequencies comparable with young mice.

265 eus accumbens shell and prefrontal cortex of aged mice to levels comparable with those observed in yo

266 and sequential cytokine delivery regimens in aged mice to restore delayed recruitment of macrophages

267 e to sepsis, the increased susceptibility of aged mice to sepsis appears not to be due to an exaggera

268 noted a dramatic decrease in the ability of aged mice to support survival and homeostatic proliferat

269 ontrast, subjecting the MuSC population from aged mice to transient inhibition of p38alpha and p38bet

270 Our data indicate that exposure of aged mice to young blood late in life is capable of reju

271 In aged mice, total Abeta levels and amyloid plaque load we

272 es in the memory Th17 compartment predispose aged mice toward the development of severe corneal epith

273 ating blood factors in plasma from exercised aged mice transferred the effects of exercise on adult n

274 These findings were recapitulated in aged mice treated with an MCD inhibitor (CBM-3001106), a

275 bsence of Pax7+ satellite cells in young and aged mice using an inducible Pax7(CreER) -R26R(DTA) mode

276 ncy results in retinal ganglion cell loss in aged mice via involvement of oxidative stress.

277 Conversely, a reduction of inflammation in aged mice via transgenic expression of alpha-1-antitryps

278 Overt tau pathology in the aged mice was accompanied by spatial memory deficits.

279 ame behavioral memory formation in young and aged mice, we examined synapse ultrastructure and molecu

280 phocytes from inflamed versus healthy middle-aged mice, we found elevated numbers of T follicular hel

281 By using multiorgan genome-wide analysis of aged mice, we found that the choroid plexus, an interfac

282 Using middle-aged mice, we modeled metabolic disease (obesity/prediab

283 cine-elicited RSV-specific CD8(+) T cells in aged mice, we used a peptide vaccine approach.

284 In contrast, the Piccolo levels in NMJs from aged mice were comparable to levels in adult mice.

285 l analysis revealed that nearly all Tregs in aged mice were of an effector phenotype (CD44(hi)CD62L(l

286 ing in intact hearts from alcohol-exposed or aged mice (where JNK2 is activated).

287 ite cell function and muscle regeneration in aged mice, whereas overexpression of Hoxa9 mimics ageing

288 s response in activated satellite cells from aged mice, which limits satellite cell function and musc

289 Synaptic transmission is degraded in aged mice, which may contribute to the decline in neural

290 D8(+) T-cell-dependent tumour elimination in aged mice, which requires IFN-gamma.

291 Additionally, investigation of aged mice with AR ablation reveals severe cortex disrupt

292 s selectively impaired in the hippocampus of aged mice with cognitive deficits.

293 r captopril on wound healing in diabetic and aged mice with further validation in older diabetic pigs

294 ear structure and function were preserved in aged mice with gain-of-function nAChRs that provide enha

295 roglia cultures and that treatment of middle-aged mice with indapamide was associated with a decrease

296 Treatment of aged mice with the nucleoside reverse transcriptase inhi

297 3 increased in adipose tissues of 28-wk-old (aged) mice with impaired beiging capability.

298 neutrophils and eosinophils were detected in aged mice, with a corresponding decrease in circulating

299 ownregulated upon wounding in both young and aged mice, with an exception of acute upregulation of mi

300 issue stem and progenitor cells in naturally aged mice without causing severe thrombocytopenia.