Sentences with phrase «seen in aged mice»

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.

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.

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).

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

Normal mice saw benefits, too: Muscles and pancreas cells healed better in middle - aged mice that got rejuvenation treatments than in mice that did not.

«This study provides the first evidence that age - related heart dysfunction can be improved even in late life via appropriate drug treatment,» added Melov, who said the treated mice saw a reduction in heart size, reduced stress signaling in heart tissues and a reduction in inflammation.

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

Elderly mice suffering from age - related heart disease saw a significant improvement in cardiac function after being treated with the FDA - approved drug rapamycin for just three months.

«It was incredible to see that in adult mice, who have gone through normal development and aging, simply overexpressing Arc with a virus restored plasticity,» says co-first author Kyle Jenks, a graduate student in Shepherd's lab.

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.»

Next, Prins exposed the mice to elevated estrogen levels for two to four months, to mimic the normal rise in estrogen seen in aging men.

After the tissue was allowed to mature for one month, the mice were given estrogen to mimic the naturally rising estrogen levels seen in aging men.

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.

«It's still too early to see if this works in humans,» says Rafael de Cabo, an investigator at the National Institute on Aging who has collaborated with Sinclair and is testing some of Sirtris's compounds in mice.

To see whether point mutations, which affect just one DNA base in mtDNA, are directly involved in aging, a team of researchers at the University of Washington in Seattle charted mtDNA mutation frequency in normal mice and «mitochondrial mutator» mice.

The researchers also did functional MRI (fMRI) studies of the mice with inhibited RbAp48 and found a selective effect in the DG, similar to that seen in fMRI studies of aged mice, monkeys, and humans.

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).

In Ames dwarrf, Snell Dwarf mice, Klotho mice, GHKO mice who have little IGF and GH; and live longer than wild - type; we see that indeed insulin and glucose / nutrient / energy pathways (which create oxidative stress through excessive nutrient via elevated glycation blood glucose creating high glycated albumin and hemoglobin), that aging is acted on by IGF through hormones, GFs, GHs, acting on insulin signals, which act on survival genes (DAF / SIRT / FOXO).

On the other hand, there are many other tissues — notably, the kidney and articular cartilage — where p16Ink4a - expressing senescent cells appear to be a contributing factor to human and murine degenerative aging, but which were not evaluated in treated or control mice in this study, and it would be of interest to see the effects of ablation of p16Ink4a - positive senescent cells.

To see if those effects might explain the link between paraquat, aging, and PD in living organisms, the team turned to genetically altered mice that the Campisi lab had developed for senescent cell studies.

The study found that the microglia cells — the immune cells of the brain — in middle - aged mice already showed altered activity seen in microglia from older mice.

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.

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.

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

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).

By the time they were in late middle age, the mice that had not been given melatonin began to develop the behavioral changes and cognitive deficits seen in Alzheimer's disease.