Sentences with phrase «aged older mice»

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.

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.

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.

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).

«When this question came up, I said, «Well, I have no idea,»» recalls Bartke, because the mice were always killed in the lab's endocrinology experiments before reaching old age.

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).

Three groups of middle - aged mice (about a year old) were studied: one group ate a normal diet, in which fewer than 30 percent of calories came from fat, while two others were fed high - calorie diets in which 60 percent of the calories came from fat.

When the huntingtin gene is deleted at an age older than four months, these mice appeared to stay healthy, despite having lost their huntingtin genes in cells all over their bodies.

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.

They found that at 6 months of age, these mice had reduced capillary density and could run only half as far as normal 6 - month - old mice.

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.

These mice survived about 600 days after exposure to infectious prions — well into old age for a mouse.

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.

Remarkably, the same healing effect was produced when B cells from older obese diabetic mice were applied to acute wounds in similarly aged, obese diabetic mice.

The mice began treatment at 30 - days - old — before any pathological or cognitive signs of AD were present — and continued until six months of age.

When the scientists blocked Treg cells from accumulating in the fat by targeting a molecule that the immune cells require, mice no longer developed type 4 diabetes in old age.

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).

Moreover, a higher proportion of germ - free mice lived to the ripe old age of 600 days, and macrophages derived from older germ - free mice maintained anti-microbial activity.

This report shows, however, that after only eight weeks of exercise, old mice experienced faster muscle repair and regained more muscle mass than those of the same age that had not exercised.

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

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.

Mice lacking the receptors also retain some youthful features into old age, such as efficient oxygen metabolism (Cell, doi.org/swb).

Those antibodies also seemed to help the brains of older mice that had aged naturally, the team found.

A protein in blood can repair age - related damage in the brains and muscles of old mice, returning them to a more youthful state.

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

Although these mice are smaller than their normally fed peers, they seem to retain their youthfulness and intellects well into their extended old age.

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.

When the research team gave old mice — the equivalent of 70 - to 80 - year - old humans — water containing an antioxidant known as MitoQ for four weeks, their arteries functioned as well as the arteries of mice with an equivalent human age of just 25 to 35 years.

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.

By 18 months — old age for a mouse — the mice from generations 3 through 6 were going grey and balding.

When Yousef injected plasma from people in their late 60s into the bodies of 3 - month - old mice — about 20 years old in human terms — the mice's brains showed signs of ageing.

Next, the researchers gave the drug to older mice that already showed signs of aging, such as muscle loss.

Older mice seem to benefit from such an arrangement, developing healthier organs and becoming protected from age - related disease.

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

(A) Isolated islets from 3 - wk - old, female, Tg - hIAPP mice were cultured in presence of different concentrations of islet extracts (IE) from old Tg - hIAPP mice, with overt diabetic pathology and age - matched WT 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 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.

Isolated islets from 3 - wk - old Tg - hIAPP, which do not exhibit IAPP aggregates at that age (Janson et al., 1996), were cultured in the presence of 1 % or 0.1 % islets extracts from old Tg or WT mice for 7 d under standard conditions, including a glucose concentration of 11 mM in the medium to reduce glucotoxicity and spontaneous aggregation of the protein (Zraika et al., 2007).

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

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

Because mice, like humans, lose bone as they age, the scientists also treated older mice with LLP2A - Ale.

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.

So the team engineered a mouse model that gradually lost the enzyme as it grew older and then bred those mice with rodents that were engineered to develop amyloid plaques from an age of 75 days.

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.).