Sentences with phrase «study in aged mice»

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.

Not exact matches

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.

In the early»90s, Bartke wrote a grant application proposing to study the giant, growth - hormone - flooded mouse as an example of accelerated aging.

«After six months, resveratrol essentially prevented most of the negative effects of the high - calorie diet in mice,» says study co-author Rafael de Cabo of the National Institute of Aging (NIA).

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 - 45In 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 - 45in 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.

«There's nothing natural about what we're doing, and adding a few tubes to a cage is not going to change that,» says Jonathan Godbout, a neuroscientist at The Ohio State University (OSU) in Columbus who studies aging and stress in mice.

At PENN - PORT, Varamini worked in the research lab of physiology professor Joseph A. Baur, studying the molecular mechanisms of aging in transgenic mice.

One study published this year in Neurobiology of Aging, from researchers at the University of Southern California, examined brain changes in mice exposed to particulate air pollution at levels commonly found near freeways.

By studying a strain of mice bred to overexpress α - synuclein via the Thy - 1 promoter, scientists have found these mice develop many of the age - related progressive motor symptoms of PD and demonstrate changes in sleep and anxiety.

«This makes it trickier to interpret the claim that the bi-maternal mice are unusually long - lived,» says Richard Miller, who studies the genetics of ageing at the University of Michigan in Ann Arbor.

In their study, the researchers showed that already at the age of six weeks in the mice with a rapid weight gain, the DPP4 gene was less methylated at four specific loci, i.e. epigenetically altered, compared to the other micIn their study, the researchers showed that already at the age of six weeks in the mice with a rapid weight gain, the DPP4 gene was less methylated at four specific loci, i.e. epigenetically altered, compared to the other micin the mice with a rapid weight gain, the DPP4 gene was less methylated at four specific loci, i.e. epigenetically altered, compared to the other mice.

«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.

Studying aging and its associated diseases has been challenging because existing vertebrate models (e.g., mice) are relatively long lived, while short - lived invertebrate species (e.g., yeast and worms) lack key features present in humans.

Studying mouse monocytes in more detail, the researchers found that the increase in TNF levels that occurs with age causes premature release of immature monocytes from the bone marrow into the blood stream.

Patricia Hunt (then working at Case Western Reserve University) was studying the endocrine environment of the aging ovary in mice.

And the trouble with extrapolating so much from mouse studies is that «nobody has actually shown over the long term how long these quote un-quote improvements persist, and we don't know whether it's broadly improving aspects of aging or it's specific to certain tissues,» said Matt Kaeberlein, a biologist who studies aging in dogs and other animal models at the University of Washington.

But this study hints that the rest periods between bouts of dieting, not the time spent cutting calories, may play an important role in nerve cell growth in mice, says Mark Mattson, a neuroscientist at the National Institute on Aging in Baltimore, Md., who wasn't involved in the study.

Historically, animal models — from fruit flies to mice — have been the go - to technique to study the biological consequences of aging, especially in tissues that can't be easily sampled from living humans, like the brain.

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.»

But without SCF, the hair in mouse models was gray, and then turned white with age, according to the study.

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.

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.

But by the age of 80 - 90 days, untreated USH3 mice in the study couldn't hear 100 decibels — akin to standing next to a running snowmobile or in a busy woodshop and not hearing anything.

But low doses of the active ingredient in cannabis, THC, might have the opposite effect on the elderly, reversing brain ageing and restoring learning and memory — at least according to studies of mice.

Yilmaz, who studies colon cancer and how it is influenced by genes, diet, and aging, decided to adapt this approach to generate colon tumors in mice.

Studying mouse models of glaucoma, Ban, Apte and their colleagues identified a molecule in the eye called growth differentiation factor 15 (GDF15), noting that the levels of the molecule increased as the animals aged and developed optic nerve damage.

In a new study in mice published in the Journal of Nutritional Biochemistry, scientists at the Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University (HNRCA) set out to determine if excess folic acid intake caused adverse changes in the immune systeIn a new study in mice published in the Journal of Nutritional Biochemistry, scientists at the Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University (HNRCA) set out to determine if excess folic acid intake caused adverse changes in the immune systein mice published in the Journal of Nutritional Biochemistry, scientists at the Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University (HNRCA) set out to determine if excess folic acid intake caused adverse changes in the immune systein the Journal of Nutritional Biochemistry, scientists at the Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University (HNRCA) set out to determine if excess folic acid intake caused adverse changes in the immune systein the immune system.

Although muscle cells did not reduce in size or number in mice lacking a protective antioxidant protein, they were weaker than normal muscle cells, researchers from the Barshop Institute for Longevity and Aging Studies at The University of Texas Health Science Center San Antonio found.

«Earlier studies have shown that vitamin E can help regulate the aging body's immune system, but our present research is the first study to demonstrate that dietary vitamin E regulates neutrophil entry into the lungs in mice, and so dramatically reduces inflammation, and helps fight off infection by this common type of bacteria,» said first author Elsa N. Bou Ghanem, Ph.D., postdoctoral scholar in the department of molecular biology and microbiology at Tufts University School of Medicine (TUSM).

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.

Image analysis studies of the IAPP staining (Fig. 3 A) show that both the percentage of islets containing IAPP aggregates (Fig. 3 E) and the load of IAPP deposits (Fig. 3 F) in the Tg / Tg group of mice progressively increased with age.

Finally, the study data suggest that RbAp48 protein mediates its effects, at least in part, through the PKA - CREB1 - CBP pathway, which the team had found in earlier studies to be important for age - related memory loss in the mouse.

The duration (20 minutes) used in the current study was based on previous work by our group demonstrating attenuation of age - related bone loss in male mice (36), but this duration is also less than the 60 - minute protocol shown to promote bone formation in the study by Jing et al. (44).

The study, conducted in postmortem human brain cells and in mice, also offers the strongest causal evidence that age - related memory loss and Alzheimer's disease are distinct conditions.

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.

To determine whether RbAp48 plays an active role in age - related memory loss, the researchers turned to mouse studies.

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.

We also study how molecular signaling, translational control, synaptic plasticity, and behavior are altered in mouse models of developmental disability, autism, aging, and Alzheimer's disease.

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.).

Among their experiments, the researchers studied beta cell signaling in mice that were modified to lack expression of the proteins and experienced insulin resistance by being placed on a high - fat diet, or aging, or becoming pregnant.

As in a number of other cases, this investigation wasn't started as a part of any aging or longevity study, and the longevity of these mice is a fortunate happenstance.

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.

This new study investigates this in old mice showing signs of age - related worsening of memory function.

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 201In 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 201in 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 201In 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 201in 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 201in 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.

The current study evaluates how CAG repeat number affects both the age of onset and the progression of disease in the R6 / 2 mouse model of Huntington's disease (Mangiarini et al., 1996) by concurrently evaluating R6 / 2 mice with either 110 or 240 CAG repeats in an F1 hybrid background (C57Bl / 6 x CBA / CaJ).

[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 micIn 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 micin similar - aged WT mice.

We tested R6 / 2 transgenic mice, a widely used genetic model of Huntington's disease (Mangiarini et al., 1996), in two studies designed to evaluate progression of the disease phenotype with age.

In comparison, the AD mice in this study were allowed to age to 20 months before being fed J147 for 3 monthIn comparison, the AD mice in this study were allowed to age to 20 months before being fed J147 for 3 monthin this study were allowed to age to 20 months before being fed J147 for 3 months.