Sentences with phrase «as in aged mice»

These analyses revealed some of the same effects of rapamycin in young mice as in aging mice (decreased CD25 + CD4 + T cells; Figure 9C), whereas other effects were not present (no decrease in CD44hi T cell frequency; Figure 9E).

Not exact matches

In 2014, highly publicized work in the laboratories of Villeda and Tony Wyss - Coray, PhD, professor of neurology at Stanford, showed that connecting the circulatory system of a young mouse to that of an old mouse could reverse the declines in learning ability that typically emerge as mice agIn 2014, highly publicized work in the laboratories of Villeda and Tony Wyss - Coray, PhD, professor of neurology at Stanford, showed that connecting the circulatory system of a young mouse to that of an old mouse could reverse the declines in learning ability that typically emerge as mice agin the laboratories of Villeda and Tony Wyss - Coray, PhD, professor of neurology at Stanford, showed that connecting the circulatory system of a young mouse to that of an old mouse could reverse the declines in learning ability that typically emerge as mice agin learning ability that typically emerge as mice age.

Instead of impairing learning and memory, as it does in young people, the drug appears to reverse age - related declines in the cognitive performance of elderly mice.

Fossils of the other new species, found in rocks of a similar age a few dozen kilometers away, suggest that creature — dubbed Vilevolodon, roughly from the Latin for «toothed glider» — was about as large as a midsized mouse.

In the early»90s, Bartke wrote a grant application proposing to study the giant, growth - hormone - flooded mouse as an example of accelerated aging.

A mouse engineered to have Alzheimer's disease and a gradual reduction in levels of the brain enzyme BACE1 stopped forming plaques (arrows in the first panel) as it aged.

The researchers then decided to see what would happen if they boosted sirtuin levels in normal mice as they aged.

Furthermore, examination of aged mice showed dramatically reduced levels of Cbf - beta in bone marrow cells, as compared to younger mice.

In addition to colitis, these mice also developed a form of colon cancer (known as colitis - associated cancer) as they aged.

And in 2001, molecular biologist Mark Sands at Washington University in St. Louis, Missouri, found a high rate of liver tumors in middle - aged mice that had been treated as newborns with a supposedly safer viral vector.

As a result, they have less than half of the fat tissue found in normal, aged mice.

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

Although we did observe positive effects on some aging traits, such as memory impairments and reduced red blood cell counts, our studies showed that similar drug effects are also seen in young mice, indicating that rapamycin did not influence these measures by slowing aging, but rather via other, aging - independent, mechanisms.»

NO BARRIER A protein in some cells that form the blood - brain barrier (light blue, as seen in this image of a mouse brain capillary) may have a hand in brain aging, a new study suggests.

As mice and humans age, levels of that protein circulating in the blood rise, Alzheimer researcher Tony Wyss - Coray at Stanford University and colleagues found.

The authors also found abnormalities in the subthalamic nucleus occur earlier than in other brain regions, and that subthalamic nucleus nerve cells progressively degenerate as the mice age, mirroring the human pathology of Huntington's disease.

Walford's new research is based on the fact that in mice and humans, the immune system malfunctions during aging, losing the ability to distinguish between healthy cells and invasive pathogens such as bacteria and viruses.

In one group of mice, he and his colleagues dosed their mothers with a synthetic compound that simulates a mild viral infection during late pregnancy; when their offspring hit early puberty at about 6 weeks of age, the young mice were exposed to unpredictable stress, such as being restrained, deprived of water, or given electric foot shocks.

As the mice aged, they became hyperactive, anxious, and antisocial, in addition to having problems with movement that mirrored patient symptoms.

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.

Nevertheless, the mutator mice showed no signs of premature aging, such as osteoporosis, balding, or reduced fertility, the team reported online 4 March in Nature Genetics.

They noted a reduction in the number of spines as the mice aged and their Alzheimer's disease progressed.

Conversely, Tg - hIAPP mice inoculated with WT pancreas homogenate (hereafter referred to as the Tg / WT group) only began to show small IAPP aggregates at around 20 wk of age (Fig. 3, A and B), in a manner similar to untreated Tg mice.

Groups of male Tg - hIAPP mice were injected i.p. at 3 wk of age with 10 % pancreas homogenate from either 12 - mo - old, male, IAPP Tg mice bearing substantial islet amyloid aggregates (as shown in Fig. 1) or from age - matched, male, WT mice not expressing hIAPP.

The discovery in mice could upend current notions about why people gain weight as they age, and could one day lead to more effective weight - loss medications.

Investigating mouse models for biological for research The congress aims to promote the International Mouse Phenotyping Consortium (IMPC) mouse lines, importance of mouse phenotyping & clinical and drug discovery collaboration, to present progresses performed by IMPC with regards CRISPR editing genome, rare diseases, microbiota and ageing pipeline, as well as illustration of examples of scientific projects about «Animal models for human diseases» and recent developments in mouse models phenotyping imamouse models for biological for research The congress aims to promote the International Mouse Phenotyping Consortium (IMPC) mouse lines, importance of mouse phenotyping & clinical and drug discovery collaboration, to present progresses performed by IMPC with regards CRISPR editing genome, rare diseases, microbiota and ageing pipeline, as well as illustration of examples of scientific projects about «Animal models for human diseases» and recent developments in mouse models phenotyping imaMouse Phenotyping Consortium (IMPC) mouse lines, importance of mouse phenotyping & clinical and drug discovery collaboration, to present progresses performed by IMPC with regards CRISPR editing genome, rare diseases, microbiota and ageing pipeline, as well as illustration of examples of scientific projects about «Animal models for human diseases» and recent developments in mouse models phenotyping imamouse lines, importance of mouse phenotyping & clinical and drug discovery collaboration, to present progresses performed by IMPC with regards CRISPR editing genome, rare diseases, microbiota and ageing pipeline, as well as illustration of examples of scientific projects about «Animal models for human diseases» and recent developments in mouse models phenotyping imamouse phenotyping & clinical and drug discovery collaboration, to present progresses performed by IMPC with regards CRISPR editing genome, rare diseases, microbiota and ageing pipeline, as well as illustration of examples of scientific projects about «Animal models for human diseases» and recent developments in mouse models phenotyping imamouse models phenotyping imaging.

Ageing XpdTTD / TTD mice develop kyphosis (curvature of the spinal column) and reduction of bone mineral density as shown in the 6 — 8 segment of the tail vertebrae counted from the pelvis (see close - up at right).

Hypothesis driven approaches to vaccinology can utilise the knowledge gained from mechanistic mouse models and our molecular understanding of intrinsic defects to human cells.5 However, caution is required when extrapolating data from murine models, as there are substantial differences between immune ageing in mice and humans.6 Nevertheless, model systems and ex vivo analyses of molecular alterations in aged human cells have identified multiple changes in the vaccination response with age and the aged immune system in general.

The researchers measured NF - κB activation in mouse brains as they aged and noted that, while the protein was barely active in the hypothalamuses of young mice, it became increasingly active as the mice got older.

Researchers have shown that lowered levels of c - myc can modestly slow aging and extend life in mice, with some evidence that this is due to effects on insulin metabolism, though there is a still a lot of investigation needed to take that as a firm conclusion.

Angiotensin II receptor type 1 (Agtr1a): Lowering Agtr1a protein levels protects mitochondrial function and modestly extends life in mice, though as for many of these methods of somewhat slowing aging there are probably many other changes to the operation of metabolism that are as yet unexplored.

GDF11: Higher levels of GDF11 have been shown to improve numerous measures of aging in mice, such as heart function, exercise capacity, and sense of smell.

As in a number of other cases, this investigation wasn't started as a part of any aging or longevity study, and the longevity of these mice is a fortunate happenstancAs in a number of other cases, this investigation wasn't started as a part of any aging or longevity study, and the longevity of these mice is a fortunate happenstancas a part of any aging or longevity study, and the longevity of these mice is a fortunate happenstance.

Oisín has shown as much as an 80 % reduction in senescent cells in cell culture and significant reductions of senescent cell burden in naturally aged mice.

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).

Similarly, using SmartCube ® technology we identified distinct behavioral changes as early as 6 - 7 weeks of age in SOD1 mice and 12 - 14 weeks for PFN1 mice.

Treatment with AFF 1 or vehicle control was initiated in mThy1 - AS mice at age 3 mo, when early sensorimotor deficits first appear — similar to the target population for the first rollout of the human vaccine.

Behaviorally, the mice with 110 CAG repeats showed a sharp decline in both rotarod and open field performance from around 4 weeks of age whereas the 240 CAG repeat mice displayed a 2 - 3 week delay in the onset of behavioral decline with a much slower progression of decline in both tasks as compared to 110 CAG repeat counterparts.

(8) Imputation of these results specifically to the animals» age - related, low - BubR1 - driven rise in p16Ink4a - expressing senescent cells was, however, limited: limited by the very nature of so - called «accelerated aging» models such as BubR1H / H, (9) and limited by the lifelong, global absence of p16Ink4a expression in the backcrossed 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.

Currently, Everon is optimizing several lead compounds: small molecules and biologics that have already demonstrated a rejuvenation effect in aging animals, as measured by a lowered mouse FI (similar FI has recently been accepted by FDA as a measure of aging in the ongoing Metformin human trial).

This early hint that age - related changes in EP2 action in microglia might be promoting some of the neuropathological features implicated in Alzheimer's was borne out in subsequent experiments for which Andreasson's team used mice genetically predisposed to get the mouse equivalent of Alzheimer's, as well as otherwise normal mice into whose brains the scientists injected either A-beta or a control solution.

Gontier and colleagues found that as mice age, Tet2 levels in the hippocampus decline, as do the epigenetic tags Tet2 makes on DNA.

Oisín's platform has shown as much as an 80 % reduction in senescent cells in cell culture and significant reductions of senescent cell burden in naturally aged mice.

Higher serum levels of pro-inflammatory factors such as interleukin - 6 and tumor necrosis factor are found in aged mice.

It should be noted, however, that while a study on senescent cell ablation in genetically normal mice would provide at least some evidence on the effect of senescent cells (and their ablation) on promoting cancer, even such a study would likely show less effect than could be anticipated in a large mammal model, since even normally - aging mice rarely suffer metastatic disease to the extent of aging humans, as sheer primary tumor volume is generally sufficient to be fatal to mice.

Methods: R6 / 2 CAG 240 (peak training at 11 weeks of age), zQ175 knock in (KI) HET (peak training at 27 weeks of age) and BAC HD (peak training at 48 weeks of age), as well as respective age - matched wild type (WT) control mice, were trained on the peak interval task (20 s interval) in which response rates during unreinforced peak trials were examined.

As the investigators note, the rapid age - related arterial stiffening and cardiac arrhythmias that appear to be at cause for the majority of deaths in BubR1H / H mice were not attenuated by ablating p16Ink4a - expressing senescent cells — but these tissues had little burden of such cells, so this finding reinforces the conclusion that the multiple aging phenotypes arrested in these mice when senescent cells were ablated is attributable specifically to the removal of their baleful influence on local tissues.

The success of the treatment in older mice, which corresponded to late adulthood in humans, is particularly important, as this would be the age that would be targeted were this method ever to be used therapeutically in people.

The congress aims to promote the International Mouse Phenotyping Consortium (IMPC) mouse lines, importance of mouse phenotyping & clinical and drug discovery collaboration, to present progresses performed by IMPC with regards CRISPR editing genome, rare diseases, microbiota and ageing pipeline, as well as illustration of examples of scientific projects about «Animal models for human diseases» and recent developments in mouse models phenotyping imaMouse Phenotyping Consortium (IMPC) mouse lines, importance of mouse phenotyping & clinical and drug discovery collaboration, to present progresses performed by IMPC with regards CRISPR editing genome, rare diseases, microbiota and ageing pipeline, as well as illustration of examples of scientific projects about «Animal models for human diseases» and recent developments in mouse models phenotyping imamouse lines, importance of mouse phenotyping & clinical and drug discovery collaboration, to present progresses performed by IMPC with regards CRISPR editing genome, rare diseases, microbiota and ageing pipeline, as well as illustration of examples of scientific projects about «Animal models for human diseases» and recent developments in mouse models phenotyping imamouse phenotyping & clinical and drug discovery collaboration, to present progresses performed by IMPC with regards CRISPR editing genome, rare diseases, microbiota and ageing pipeline, as well as illustration of examples of scientific projects about «Animal models for human diseases» and recent developments in mouse models phenotyping imamouse models phenotyping imaging.