Furthermore, examination of
aged mice showed dramatically reduced levels of Cbf - beta in bone marrow cells, as compared to younger mice.
Not exact matches
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.
This image
shows the discovery by researchers that induction of partial cellular reprogramming improved muscle regeneration in
aged mice.
The cardiovascular system, which often fails and causes early death in these prematurely
aging mice, also
showed improvements in structure and function.
Shown are a
mouse with a premature
aging disease called progeria (left) and a
mouse with progeria that got reprogramming treatments (right).
Mice that make extra of the protein
show signs of premature
aging.
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
mice.
A low - fat diet in combination with limited caloric consumption prevents activation of the brain's immune cells — called microglia — in
aging mice,
shows research published today in Frontiers in Molecular Neuroscience.
«We also carried out behavioral assessments which
showed the treated
mice spent more time on running wheels than the
mice who
aged without intervention.»
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.
In marked contrast to the widely held notion that the insulin - producing pancreatic beta cell loses function with wear and tear, the researchers now
show that
mouse and human beta cells are fully functional at advanced
age.
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.
«Sleep - deprived
mice show connection with diabetes,
age.»
Longo also knew of research by molecular biologist John Kopchick at Ohio University, which
showed that
mice with a mutation in their growth hormone receptor gene lived 40 percent longer than normal
mice — the equivalent of an average American living to
age 110.
By examining first pregnancies in
aged mice, the team
showed that, for
mice as for humans, the risk of complications increases with
age.
«Gut microbes contribute to
age - associated inflammation,
mouse study
shows.»
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.
Strikingly, the germ - free
mice did not
show an
age - related increase in intestinal permeability or in levels of bacterial products or pro-inflammatory cytokines in the bloodstream, in contrast to conventionally raised
mice.
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.»
These
mice start
showing tau tangles at around 6 months of
age and exhibit some neuronal damage by 9 months.
By the time this strain of genetically modified
mice reaches 9 months of
age, the hippocampus — a part of the brain important for memory — typically is visibly shrunken and
shows dying neurons.
In the past five years, that compound, resveratrol, has been
shown to slow
aging in worms, flies, and
mice.
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.
Studies out this summer from Sinclair and others
show that
mice given resveratrol have reduced
aging of the heart, slower cataract development, and better bone density.
A group of scientists led by Sebastian Jessberger of the Brain Research Institute
showed now that also the stem cells of the adult
mouse brain asymmetrically segregate
aging factors between the mother and the daughter cells.
For researchers working on animal models, it
shows that the
age of male
mice can influence the behavior of the offspring, so this should be a consideration when they are used to mate.
The researchers discovered that
mice with genetic mutations that stop this endocannabinoid system from working properly
age faster than normal
mice, and
show more cognitive decline.
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.
Nevertheless, the mutator
mice showed no signs of premature
aging, such as osteoporosis, balding, or reduced fertility, the team reported online 4 March in Nature Genetics.
But
mice engineered to have hundreds of times more of these mutations than average
showed no signs of premature
aging, indicating that scientists are going to have to look elsewhere for their culprit.
«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).
Next, the researchers gave the drug to older
mice that already
showed signs of
aging, such as muscle loss.
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.
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).
Conversely, Tg - hIAPP
mice inoculated with WT pancreas homogenate (hereafter referred to as the Tg / WT group) only began to
show small IAPP aggregates at around 20 wk of
age (Fig. 3, A and B), in a manner similar to untreated Tg
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.
A study by Stephen Abolins, Mark Viney and colleagues of the immune ecology of wild house
mice — the same species as the lab
mouse —
shows that their immune state is promoted by individuals» body condition and constrained by their
age.
Here, we've caused
age - related memory loss in the
mouse, and we've
shown it to be relevant to human
aging.»
In
mice predisposed to the disease, we
showed that these fatty acids accumulate very early on, at two months of
age, which corresponds to the early twenties in humans.
The first part of the study
showed that giving birth multiple times was a significant contributor to obesity regardless of
age, with
mice who gave birth multiple times being up to 45 percent heavier than those who had a single litter at the same
age that the first animals had their fourth.
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).
Researchers have
shown that lowered levels of c - myc can modestly slow
aging and extend life in
mice, with some evidence that this is due to effects on insulin metabolism, though there is a still a lot of investigation needed to take that as a firm conclusion.
GDF11: Higher levels of GDF11 have been
shown to improve numerous measures of
aging in
mice, such as heart function, exercise capacity, and sense of smell.
Oisín has
shown as much as an 80 % reduction in senescent cells in cell culture and significant reductions of senescent cell burden in naturally
aged mice.
This new study investigates this in old
mice showing signs of
age - related worsening of memory function.
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.
Mice that had been eating a ketogenic diet performed at least as well on memory tests at old age as they did at middle age, while mice eating the normal diet showed an expected age - associated decl
Mice that had been eating a ketogenic diet performed at least as well on memory tests at old
age as they did at middle
age, while
mice eating the normal diet showed an expected age - associated decl
mice eating the normal diet
showed an expected
age - associated decline.
In addition, 110 CAG
mice exhibited tremors at rest at early
ages, but the 240 CAG
mice only
showed tremors at later
ages and only after manipulation.
Behaviorally, the
mice with 110 CAG repeats
showed a sharp decline in both rotarod and open field performance from around 4 weeks of
age whereas the 240 CAG repeat
mice displayed a 2 - 3 week delay in the onset of behavioral decline with a much slower progression of decline in both tasks as compared to 110 CAG repeat counterparts.
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).