Sentences with phrase «treated aged mice»

To examine cardiac aging phenotypes, we performed echocardiography in rapamycin - and vehicle - treated aged mice and young controls.

We also measured cross-sectional muscle fiber areas in quadriceps femoris muscle of rapamycin - or vehicle - treated aged mice and corresponding young controls (16 - and 25 - month cohorts; Figure 4, G and H), which showed the expected aging - associated decrease in cross-sectional muscle fiber area.

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

Not exact matches

An MIT - led research team has now found that it can reverse this age - related endurance loss in mice by treating them with a compound that promotes new blood vessel growth.

«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.

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.

«We also carried out behavioral assessments which showed the treated mice spent more time on running wheels than the mice who aged without intervention.»

The identification of factors that slow the age - dependent deterioration of the neurogenic niche in mice may constitute the basis for new methods of treating age - related neurodegenerative and neurovascular diseases.

The experimental drug J147 is something of a modern elixir of life; it's been shown to treat Alzheimer's disease and reverse aging in mice and is almost ready for clinical trials in humans.

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.

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

Another group of mice was treated in older age, after cataracts had already set in.

Again, then, there is significant evidence consistent with a role of cellular senescence in age - related lipodystrophy and lipoatrophy, and for the benefits observed in treated mice in these studies to translate into aging humans.

Results from this two - day water maze show that AD mice take considerably longer to find the hidden platform on Day 2 than AD mice treated with J147 for three months (Figure 1A), demonstrating that J147 significantly improved the spatial navigational memory in aged, transgenic AD mice.

(6) This is consistent with the deleterious effect of such cells on tissue function, and with the researchers» conclusion that «the observed improvements in skeletal muscle and fat of late - life treated 10 - month - old BubR1H / H; INK - ATTAC - 5 mice reflect attenuated progression of age - related declines rather than a reversal of ageing».

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).

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.

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.

Relative to both control cohorts of the same age, 9 - 10 mo old treated mice exhibited dramatically more youthful tissues.

Figure 1: Amelioration of «Premature Aging» Phenotypes in Treated and Untreated BubR1H / H; INK - ATTAC 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 mice.

C57BL6 / J male mice aged eight weeks were assigned to five groups, 12 mice per group, and treated with compounds in their food for two weeks.

(C) Levels of another neurotrophic factor, BDNF, both pro and mature, are also increased in the hippocampus of J147 treated aged huAPP / PS1 mice.

(D) The ratio of pro- to mature BDNF is decreased in aged huAPP / PS1 mice treated with J147.

LA JOLLA — The experimental drug J147 is something of a modern elixir of life; it's been shown to treat Alzheimer's disease and reverse aging in mice and is almost ready for clinical trials in humans.

By the age of 9 - 10 mo, neurpathology was advanced in vehicle - treated animals, but it was clear that AFF 1 had afforded substantial protection to treated mice.

Figure 3F shows that J147 significantly increased the level of Egr3 in the hippocampus of J147 - treated aged AD mice compared to control AD mice.

The mice used in all these the studies were treated with memantine from a very young age, and we don't know what would happen if the mice received it only after they got sick - which is how most human patients are treated.

Treated mice received the benefits of exercise just as mice half their age.