Sentences with phrase «increased in aged mice»

Analysis of escape latencies (Figure 3B) during training indicated significant effects of aging and, possibly, rapamycin, such that escape latencies were increased in aged mice and were decreased by rapamycin treatment (P = 0.0021, P = 0.0548, and P = 0.2419 for age, treatment, and age / treatment interaction, respectively, 3 - way ANOVA with age and treatment as between - subjects factors and training day as within - subjects factor).

Not exact matches

After publishing the Nature paper on the Ames dwarf's increased longevity, Bartke secured a $ 50,000, 1 - year NIH grant to further investigate aging in the mutant mouse.

Studying mouse monocytes in more detail, the researchers found that the increase in TNF levels that occurs with age causes premature release of immature monocytes from the bone marrow into the blood stream.

With increasing age, the proteins accumulate in the brains of fruit flies, mice, and humans.

The researchers then confirmed that the number of singly paired chromosomes — also called univalents — was higher in older mouse and even human egg cells, indicating that age - related segregation errors could be tracked back to increased numbers of prematurely separated chromosome pairs.

There is increased ER stress in the pancreas of aged mice.

In an attempt to increase sensitivity for sepsis, Canaan aged these FAT10 knockout mice and made the discovery that mice lacking the gene were lean and aged more slowly.

By examining first pregnancies in aged mice, the team showed that, for mice as for humans, the risk of complications increases with age.

Ret is not an unknown factor for the Martinsried - based neurobiologists: «We already succeeded in demonstrating a few years ago in mice that neurons without the Ret receptor die prematurely and in greater numbers with increasing age,» says Klein.

Strikingly, the germ - free mice did not show an age - related increase in intestinal permeability or in levels of bacterial products or pro-inflammatory cytokines in the bloodstream, in contrast to conventionally raised mice.

Studying mouse models of glaucoma, Ban, Apte and their colleagues identified a molecule in the eye called growth differentiation factor 15 (GDF15), noting that the levels of the molecule increased as the animals aged and developed optic nerve damage.

Image analysis studies of the IAPP staining (Fig. 3 A) show that both the percentage of islets containing IAPP aggregates (Fig. 3 E) and the load of IAPP deposits (Fig. 3 F) in the Tg / Tg group of mice progressively increased with age.

The researchers have identified a protein — RbAp48 — that, when increased in aged wild - type mice, improves memory back to that of young wild - type mice.

The researchers tested their theory by orally administering a drug that inhibits DNA - PK and found that, in addition to preventing weight gain in the mice, the inhibitor drug boosted mitochondrial content in skeletal muscle, increased aerobic fitness in obese and middle aged mice, and reduced the incidence of obesity and type - 2 diabetes.

The compound increased bone tissue in the older mice and prevented age - related bone loss.

Although of course there are a number of caveats since mice can be cured from cancer at higher rates, they don't suffer from some of our diseases, they are sensitive to being handled (if grabbing them can shorten their lifespan through stress, the mouse version of standard human medical care may do the same), so I guess that increases in maximum lifespan are indeed the only reliable indicator that an intervention is impacting age - related mortality.

Previous studies in the mouse BACHD model (6 month old), reported an age - dependent increase in mean firing rate of GP neurons and decrease in the mean firing rate of STN neurons in vitro (D.J. Surmeier, Northwestern Univ.) and in vivo (James Tepper, Rutgers Univ.).

Adenylyl Cyclase Type 5 (AC5): Knockout of AC5 extends life in mice, with the most plausible mechanism being increased resilience of the cardiovascular system to the various slings and arrows of aging.

In another experiment, the researchers used viral gene transfer and increased RbAp48 expression in the DG of aged micIn another experiment, the researchers used viral gene transfer and increased RbAp48 expression in the DG of aged micin the DG of aged mice.

NRF2 / SKN - 1: Increased levels of NRF2 in mice or its homolog SKN - 1 in nematodes results in slower aging and modestly extended life spans - normally NRF2 levels decline with age.

Our data suggest that the reduction in soluble Aβ levels in the hippocampus of treated, aged AD mice compared to control AD mice by J147 is due to an effect on the APP processing pathway as J147 decreased the protein level of the BACE enzyme leading to an increase in APP levels (Figure 2D, E).

Figure 3E demonstrates that treatment with J147 significantly increased levels of this protein in aged AD mice.

[19] In the current study, [15] PDGF - AS mice exhibited an increased number and intensity of areas staining for reactive microglia (using Iba1) and astroglia (using GFAP), but vaccination with AFF 1 prevented nearly all of this disease - associated excess, with treated animals exhibiting only the burden of reactive glia present in similar - aged WT micIn the current study, [15] PDGF - AS mice exhibited an increased number and intensity of areas staining for reactive microglia (using Iba1) and astroglia (using GFAP), but vaccination with AFF 1 prevented nearly all of this disease - associated excess, with treated animals exhibiting only the burden of reactive glia present in similar - aged WT micin similar - aged WT mice.

(C) Levels of another neurotrophic factor, BDNF, both pro and mature, are also increased in the hippocampus of J147 treated aged huAPP / PS1 mice.

Treatment of aged, transgenic huAPP / PS1 mice with J147 significantly increased the amount of phosphorylated CREB in the entorhinal cortex of these mice (Figure 3H) but not in the hippocampus (data not shown).

Herein, we demonstrate that dietary deficiency in folate and vitamin E increased PS - 1 expression in juvenile and adult normal C57B1 / 6J and ApoE - / - mice and in aged normal mice.

Figure 3F shows that J147 significantly increased the level of Egr3 in the hippocampus of J147 - treated aged AD mice compared to control AD mice.

J147 treatment of aged huAPP / PS1 mice increases the expression levels of several proteins involved in neurotrophin signaling.

Potential projects include identifying common pathways that modify retinal degenerative disease from a large collection of actively maintained mouse models; determining molecular networks implicated in pathological disruption of the retinal pigment epithelium; identifying molecular pathways that regulate postnatal ocular growth; and using mouse models to assess the pathogenic role of gene variants that increase the risk of age - related macular degeneration as identified by human genome - wide association studies.

Aging tau KO mice to 23 months resulted in cardiac hypertrophy with significantly attenuated left atrial contractility, increased blood pressure, and sensitivity of isolated mesenteric arteries to angiotensin II contraction and isoprenaline relaxation compared to their younger counterparts.

This modification is of special interest to p53 - dependent anti-senescence and pro-longevity functions because genetically engineered mice with p53 serine18 mutated to alanine (p53S18A) show increased ROS levels, metabolic stress, tumor frequency, premature aging symptoms and defects in regulation of a subset of p53 target genes that include sestrins.

Thus, chronically increased p53 activity causes premature aging in mice, whereas transgenic mice with extra copies of p53 and ARF genes under normal regulation show tumor resistance and extended life span.

Although we can not rule out that exercise might also increase hippocampal progranulin in 2 - to 3 - month - old Grn + / − mice, there is no data that an increase of this magnitude (only 10 — 15 %) restricted to hippocampus would be sufficient to produce functional improvement, and the fact that the effect is not sustained even until ∼ 4 months of age makes it highly unlikely to yield any sustained benefit after onset of functional changes between 6 and 12 months.

At the University of Arizona, SENS Research Foundation is funding proof - of - concept research to restore the health of the immune system in aging mice, by simultaneously increasing the ability to produce new killer T - cells while making room for them by purging defective cells from the system.

In one set of experiments, when the scientists boosted insulin resistance by giving mice a compound that cuts insulin signaling, they saw increased expression of several markers of aging in beta cellIn one set of experiments, when the scientists boosted insulin resistance by giving mice a compound that cuts insulin signaling, they saw increased expression of several markers of aging in beta cellin beta cells.

These experiments were adequately powered to detect even minor increases in progranulin, and argue against the potential for progranulin - mediated benefits of exercise in Grn + / − mice at this age.

Three recent experimental studies focused on low consumption / exposure.949596 In one study, 29 smokers each consumed a single cigarette, immediately after which they had a significant decrease in blood vessel output power and significant increase in blood vessel ageing level and remaining blood volume 25 minutes later, as markers of atherosclerosis.94 In another study, human coronary artery endothelial cells were exposed to the smoke equivalent to one cigarette, which led to activation of oxidant stress sensing transcription factor NFR2 and up - regulation of cytochrome p450, considered to have a role in the development of heart disease.95 These effects were not seen when heart cells were exposed to the vapour from one e - cigarette.95 A study exposed adult mice to low intensity tobacco smoke (two cigarettes) for one to two months and found adverse histopathological effects on brain cells.In one study, 29 smokers each consumed a single cigarette, immediately after which they had a significant decrease in blood vessel output power and significant increase in blood vessel ageing level and remaining blood volume 25 minutes later, as markers of atherosclerosis.94 In another study, human coronary artery endothelial cells were exposed to the smoke equivalent to one cigarette, which led to activation of oxidant stress sensing transcription factor NFR2 and up - regulation of cytochrome p450, considered to have a role in the development of heart disease.95 These effects were not seen when heart cells were exposed to the vapour from one e - cigarette.95 A study exposed adult mice to low intensity tobacco smoke (two cigarettes) for one to two months and found adverse histopathological effects on brain cells.in blood vessel output power and significant increase in blood vessel ageing level and remaining blood volume 25 minutes later, as markers of atherosclerosis.94 In another study, human coronary artery endothelial cells were exposed to the smoke equivalent to one cigarette, which led to activation of oxidant stress sensing transcription factor NFR2 and up - regulation of cytochrome p450, considered to have a role in the development of heart disease.95 These effects were not seen when heart cells were exposed to the vapour from one e - cigarette.95 A study exposed adult mice to low intensity tobacco smoke (two cigarettes) for one to two months and found adverse histopathological effects on brain cells.in blood vessel ageing level and remaining blood volume 25 minutes later, as markers of atherosclerosis.94 In another study, human coronary artery endothelial cells were exposed to the smoke equivalent to one cigarette, which led to activation of oxidant stress sensing transcription factor NFR2 and up - regulation of cytochrome p450, considered to have a role in the development of heart disease.95 These effects were not seen when heart cells were exposed to the vapour from one e - cigarette.95 A study exposed adult mice to low intensity tobacco smoke (two cigarettes) for one to two months and found adverse histopathological effects on brain cells.In another study, human coronary artery endothelial cells were exposed to the smoke equivalent to one cigarette, which led to activation of oxidant stress sensing transcription factor NFR2 and up - regulation of cytochrome p450, considered to have a role in the development of heart disease.95 These effects were not seen when heart cells were exposed to the vapour from one e - cigarette.95 A study exposed adult mice to low intensity tobacco smoke (two cigarettes) for one to two months and found adverse histopathological effects on brain cells.in the development of heart disease.95 These effects were not seen when heart cells were exposed to the vapour from one e - cigarette.95 A study exposed adult mice to low intensity tobacco smoke (two cigarettes) for one to two months and found adverse histopathological effects on brain cells.96

Six weeks of wheel running (A) failed to increase frontal cortex progranulin mRNA (B) or hippocampal progranulin protein (C) in either solo - or group - housed wild - type mice aged 3 — 6 months.

In line with the behavioral data, our whole brain TissueCyte ® based analyses suggests that younger mice (∼ 4 - 5 months) exhibit very sparse parenchymal plaques while aged mice (> 7 months) show a clear progression in the number / size of plaques and display differential increases in regional plaque load number / sizIn line with the behavioral data, our whole brain TissueCyte ® based analyses suggests that younger mice (∼ 4 - 5 months) exhibit very sparse parenchymal plaques while aged mice (> 7 months) show a clear progression in the number / size of plaques and display differential increases in regional plaque load number / sizin the number / size of plaques and display differential increases in regional plaque load number / sizin regional plaque load number / size.

Estradiol increased performance in young and aged mice under minimized organizational demand, but failed to improve the age - associated memory impairment and diminished performance in young mice under high organizational demand.

Specifically, by using the NeuroCube ® system to measure gait deficits, we found that SOD - 1 mice showed a reduction in step and stride length and an increase in stride, stand and swing duration compared to WT mice, which was evident as early as 8 weeks and progressed with age.

Using AI and Computer Vision Techniques to Determine Age and Assess the Effect of Therapies Against Aging in Mice, Increasing the Pace of Research.

In general APP / PS1 mice perform worse than the tg 2576 mice, except in the investigation of social interaction, where tg 2576 mice progress with increased interaction, but the phenotype of the APPPS1 mice is closer to normal situation with increasing agIn general APP / PS1 mice perform worse than the tg 2576 mice, except in the investigation of social interaction, where tg 2576 mice progress with increased interaction, but the phenotype of the APPPS1 mice is closer to normal situation with increasing agin the investigation of social interaction, where tg 2576 mice progress with increased interaction, but the phenotype of the APPPS1 mice is closer to normal situation with increasing age.

Second, in the 16 - month cohort, rapamycin increased plasma glucose levels (which decreased in aged mice).

However, rapamycin also increased exploratory activity in young mice in our study, indicative of another aging - independent effect, rather than an effect on aging per se.

In aging mice, an increase in heat shock proteins help delay aging and improves cognitive functioIn aging mice, an increase in heat shock proteins help delay aging and improves cognitive functioin heat shock proteins help delay aging and improves cognitive function.

Gene therapy in old mice has been shown to cause to a 27 % increase in strength, along with regeneration of aging muscle.

The landmark 2013 study by Dr. Sinclair demonstrated that supplementation with NMN increased levels of NAD + and reversed age related degeneration in mice, giving older mice the muscle capacity, endurance and metabolism of much younger mice — the «equivalent of a human 60 year old becoming more like a 20 year old» (24).

At 8 months of age, both DIO and DR groups had increased hyperglycemic response during a glucose tolerance test, which was normalized in 16 - month - old mice.

In the same way, whereas NR supplementation increased muscle stem cell number in aged mice, thereby enhancing mitochondrial function and muscle strength, it reduced the expression of cell senescence and apoptosis markers [233]; the state of senescence is important to protect against carcinogenesis [234In the same way, whereas NR supplementation increased muscle stem cell number in aged mice, thereby enhancing mitochondrial function and muscle strength, it reduced the expression of cell senescence and apoptosis markers [233]; the state of senescence is important to protect against carcinogenesis [234in aged mice, thereby enhancing mitochondrial function and muscle strength, it reduced the expression of cell senescence and apoptosis markers [233]; the state of senescence is important to protect against carcinogenesis [234].