Sentences with phrase «in aging mice»

A study by researchers from Harvard Medical School in conjunction with the National Institute on Aging, published in December 2013 in CELL, demonstrated that mitochondrial dysfunction (a hallmark of aging) in aging mice is due to a disruption in sirtuin1 dependent nuclear mitochondrial communication.

A companion study published by the Buck Institute for Research on Aging in the same issue of Cell Metabolism shows that a ketogenic diet extends longevity and improves memory in aging mice.

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

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).

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.

Citation: Ketogenic diet reduces mid-life mortality and improves memory in aging mice DOI: 10.1016 / j.cmet.2017.08.004

In recent years, researchers have developed so - called «senolytic» drugs that wipe out senescent cells in aging mice and mouse models of age - related disease, exploiting the high dependence of these cells on specific biochemical survival pathways.9, 10 In these studies, senolytic drugs have restored exercise capacity9 and formation of new blood and immune precursor cells11 in aging mice to near youthful norms, and prevented or treated mouse models of diseases of aging like osteoarthritis, 12 fibrotic lung disease, 13 hair loss, 14 atherosclerosis, 15,16 and age - related diseases of the heart itself.9 UNITY Biotechnology is leading a growing charge toward the clinic, with human clinical trials expected to begin in 2019.

The team examined tissues in mice for cellular stress following acute SD, and they also looked for cellular stress in aging mice.

A low - fat diet in combination with limited caloric consumption prevents activation of the brain's immune cells — called microglia — in aging mice, shows research published today in Frontiers in Molecular Neuroscience.

These mice performed better than their normal counterparts on learning tests well into old age, and their brains did not exhibit the decline in neurogenesis typically seen in aged mice.

«And at the higher dose, we saw a rescue of the neural stem cell pool in aged mice.»

This image shows the discovery by researchers that induction of partial cellular reprogramming improved muscle regeneration in aged mice.

A genetic switch linked to memory impairment in ageing mice has been flipped back on, restoring failing brains to a more youthful state.

Additionally, the team found that induced lifelong overexpression of Nampt, an enzyme important in making NAD, prevented the natural decline in NAD and partially preserved exercise capacity in aged mice.

The GDF11 protein commonly found in the blood of young mice (the same protein that enhanced neurogenesis in aged mice) and placed in individual older mice was thought to have the same reversal effect on hypertrophy; however, more recent research suggests another molecule besides GDF11 may be at work.

However, when the researchers used drugs or mouse mutations that reduced the number of monocytes or removed TNF, they were able to restore antibacterial immunity in aged mice.

In aged mice with diabetes (represented on the right), Tregs are overexpressed in fat tissue and trigger insulin resistance.

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

«High folic acid intake in aged mice causes a lowered immune response.»

Their study in aged mice indicates that high folic acid intake causes lowered immune function because natural killer (NK) cells, a particular type of immune cell, are less effective.

«The first question was whether RbAp48is downregulated in aged mice,» said lead author Elias Pavlopoulos, PhD, associate research scientist in neuroscience at CUMC.

This effect of RbAp48 inhibition on the DG was accompanied by defects in molecular mechanisms similar to those found in aged mice.

The current study reports neurogenesis (neuron creation) occurred in the spinal cords of both adult and aged (over one - year old) mice of both sexes, although the response was much weaker in the aged mice, Dr. Zhang said.

Development of diet - induced fatty liver disease in the aging mouse is suppressed by brief daily exposure to low - magnitude mechanical signals

Loss of responsiveness to melatonin in the aging mouse suprachiasmatic nucleus.

Outflow of cerebrospinal fluid is lymphatic - specific and reduced in aged mice Steven Proulx, ETH Zurich

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

Peripheral T cell diversity is virtually constant in the young, but is invariably reduced in aged mice and humans.

We demonstrated that this device could reduce the KLRG1 - positive CD8 cell count in aged mouse blood by a factor of 7.3 relative to the total CD8 cell compartment, reaching a level typically seen only in very young animals.

c - Fos imaging of testing - induced brain activations showed that the deterioration of young memory was associated with dentate gyrus dysconnectivity, reminiscent of that seen in aged mice.

SAN FRANCISCO, CA — A new study from the Gladstone Institutes has revealed a way to alleviate the learning and memory deficits caused by apoE4, the most important genetic risk factor for Alzheimer's disease, improving cognition to normal levels in aged mice.

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

Few of the tested effects of rapamycin in our dataset were seen only in aged mice, not in young animals (RER, fat mass, γδ T cells, and CD44hi T cells); however, previous reports have shown aging - independent effects of mTOR inhibition on CD44 expression in T lymphocytes and fat mass (30, 31, 34).

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).

We therefore sought to determine whether rapamycin suppresses carcinogenesis in our aging mouse cohorts.

Co-enzyme q10 supplementation improves ovarian response and mitochondrial function in aged mice [abstract].

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 [234].

Not exact matches

It is dominated by the far - seeing genius of Josh Boger, who at age 7 does experiments in a lab above his parents» garage (including sending a hapless mouse soaring aloft on a Hindenberg - type contraption he rigs up).

Making that mistake is even more costly in an age of increasingly short attention spans and technological tools that make it easy to find some other diversion with a quick click of the computer mouse or the swipe of a finger on a smartphone.

A team led by David Sinclair of the University of New South Wales published a study in Cell, saying that they have actually reversed mice's aging process.

I ask a friend of mine, aged six, and she thinks about this For a whole minute, looking down in the grass for words, And she says, The time I tried to make a coat for a mouse From spider - webs.

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.

Dr. Issa's team made their discovery after first examining methylation patterns on DNA in blood collected from individuals of different ages for each of three species — mouse, monkey, and human.

Similar research since has found what may be the genetic signatures of Norwegian Viking Age mice in modern populations on the Azores, an island chain more than 900 miles west of Portugal.

Mice ranged in age from a few months to almost three years, monkeys from less than one year to 30 years, and humans from age zero to 86 years (cord blood was used to represent age zero).

In The EMBO Journal, they reported that NAD levels decreased with age in the mouse hippocampus, a vital region of the brain for cognitioIn The EMBO Journal, they reported that NAD levels decreased with age in the mouse hippocampus, a vital region of the brain for cognitioin the mouse hippocampus, a vital region of the brain for cognition.

Even more striking, the gene - expression pattern in the hippocampi of THC - treated aged mice was radically different from that of untreated elderly mice.

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.

Although stem cells in the hypothalamus create new neurons throughout life, the team noticed that mice start losing them in middle age — about 10 or 11 months old.

Partial reprogramming of cells within prematurely aging mice's bodies extended the rodents» average life span from 18 weeks to 24 weeks, researchers report December 15 in Cell.