Sentences with phrase «young mice age»

But the younger mice age prematurely.

Not exact matches

http://edition.cnn.com/2014/05/05/health/young-blood-mice-aging/index.html Scientists have recently found that giving old mice transfusions of young mice blood can reverse the aging process, human trials coming soon.

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 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.

The researchers conducted a series of micromanipulations on the eggs of mice between the ages of 6 and 12 weeks (young) and 60 - week - old mice (old).

To find out more about what underlies the cognitive decline that occurs with ageing, André Fischer of the European Neuroscience Institute in Göttingen, Germany, and colleagues analysed DNA from the brains of both young and old mice that had been set tasks involving learning and memory.

In this study, researchers analyzed ovarian tissue from populations of reproductively «young» (equivalent to women in their early twenties) and «old» mice (equivalent to women ages 38 - 45).

Since most grants are usually only for a four - to five - year period, using younger mice is not only less expensive, but it avoids the delay of waiting for an animal to age.

Part of the problem, he says, is that the incidence of many human chronic diseases rises with age, yet many researchers prefer using young mice because of the pressures of being published and getting funding.

Then, he found that mice lacking Klotho died young, after developing arteriosclerosis and other age - related conditions much earlier than normal (Science, 7 November 1997, p. 1013).

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.

Joseph Castellano at Stanford University in California and his colleagues discovered this by collecting blood from people at three different life stages — babies, young people around the age of 22, and older people around the age of 66 — and injecting the plasma component into mice that were the equivalent of around 50 years old in human years.

GDF - 11, which regulates the growth of spinal and olfactory (smell) receptors, is produced abundantly in young mice, but production drops off with age.

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

Among the mice that received no THC, the middle - aged and elderly animals did far worse than the young ones.

To find out, his team gave young, middle - aged and elderly mice a steady but low dose of THC.

In a chronic sleep deprivation experiment, young mice were sensitized to insulin and had improved control of their blood sugar, whereas aged animals became hyperglycemic and failed to maintain appropriate plasma insulin concentrations.

At young adulthood, Larsson's mice resembled those three times their age, with bone and muscle loss, heart disease — even baldness.

Its concentration was low and steady at young ages - within the known critical period for mice — and ramped up with age.

The mice appear younger and more robust than comparably - aged normal mice, have better muscle tone, and do not develop age - related tumors.

One mode of aging transmission is to give genetically identical mice transfusions of young or old blood.

One substance in the blood of old mice, a protein called Beta ‑ 2 ‑ microglobulin, or B2M, seemed to prematurely age the young ones, Villeda and colleagues reported last year in Nature Medicine (SN: 8/8/15, p. 10).

Overexpressing a single gene called Arc rejuvenates the visual cortex of middle - age mice, making them as plastic as younger mice.

Enter a mutant mouse strain that is afflicted at a young age with many of the diseases common to older humans.

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.»

This visual abstract represents the findings of Thevaranjan et al. who, using young and old germ - free and conventional mice, demonstrate that age - related microbiota changes drive intestinal permeability, age - associated inflammation, and decreased macrophage function.

Changes in muscle repair with aging were determined by injecting the old mice and young mice (neither group exercised) with snake venom commonly used to induce muscle injury in rodent studies.

Fractured shin bones of old mice healed faster and better when the rodents were joined to young mice than to mice their own age.

According to the researcher, who is in the closing stages of her doctorate thesis, the measurements show that in several parameters mice expressing the risk factor for Alzheimer's «age» metabolically at a relatively young age.

Old blood can prematurely age the brains of young mice, and scientists may now be closer to understanding how.

To find out, the team gave young (2 - month - old), middle - aged (12 - month - old) and elderly (18 - month - old) mice a steady dose of THC.

But now that we know what kinds of changes occur as these cells age, we can ask which of these changes reverse themselves when an old cell goes back to becoming a young cell» — as appeared to be the case when tissues of older mice were exposed to blood from younger mice.

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.

Their younger cousins recovered fine, as did older mice with telomerase intact, but more than half of the aged, telomere - depleted mice died from the treatment.

But she notes that studies in young knock - out mice may not predict the helpfulness of PlGF and similar molecules in healing fractures in humans of all ages.

The effects of blood on ageing were first discovered in experiments that stitched young and old mice together so that they shared circulating blood.

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.

Next, Abadir and colleagues compared the effects of different concentrations of losartan and valsartan on young diabetic and aged mice during the proliferation / remodeling phase of wound healing, which involves the regrowth of normal tissue.

A 36 - hour coculture of aged HSCs (from 18 - 24 month - old mice) with young MSCs (from 6 - 8 week - old mice) reversed signs of aging in HSCs

Vascular and neurogenic rejuvenation of the aging mouse brain by young systemic factors.

Now, new research from the laboratory of Vaijayanti P. Kale (National Centre for Cell Science, Pune, Maharashtra, India) has described a fascinating new approach to return lost functionality to aged mouse HSCs: the transfer of microvesicles (MVs) containing positive regulators of autophagy derived from young mesenchymal stem cells (MSCs)[6].

The researchers compared one group of mice that gave birth four times with a second group of mice that gave birth only once, some of these at the same age that the first group had its fourth litter and some at a younger age.

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.

They observed that mice with defective Mdmx developed very aggressive lymphomas at a very young age.

In fact, in the case of one type of age - related memory loss — again, distinct from Alzheimer's — researchers were able to restore memory function in mice so that it was comparable to that of young mice.

Vascular dysfunction in young, mid-aged and aged mice with latent cytomegalovirus infections.

Interestingly, we detected upregulation of p16 and p15 in Polycomb - null skin epithelial stem cells in young mice where it is normally detected only in aged animals.

Using a technique called parabiosis, in which the vascular systems of two mice are surgically connected, Villeda's lab had previously discovered that infusing old mice with the blood of younger mice leads to brain rejuvenation, including improvements in learning and memory, while infusions of old blood cause premature brain aging in young mice.

To find out if the loss of Tet2 in aging could directly cause cognitive decline, the researchers used a technique called RNAi to block Tet2 activity in the hippocampi of young adult mice.

Aged mutant amyloid precursor protein mice with established disease showed a near complete restoration in levels of synaptic and neuronal proteins after exposure to young blood in parabiosis (synaptophysin P =.02; calbindin P =.02) or following intravenous plasma administration (synaptophysin P <.001; calbindin P =.14).