These analyses revealed some of the same effects of rapamycin in young mice
as in aging mice (decreased CD25 + CD4 + T cells; Figure 9C), whereas other effects were not present (no decrease in CD44hi T cell frequency; Figure 9E).
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 ag
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 ag
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 ag
in learning ability that typically emerge
as mice age.
Instead of impairing learning and memory,
as it does
in young people, the drug appears to reverse
age - related declines
in the cognitive performance of elderly
mice.
Fossils of the other new species, found
in rocks of a similar
age a few dozen kilometers away, suggest that creature — dubbed Vilevolodon, roughly from the Latin for «toothed glider» — was about
as large
as a midsized
mouse.
In the early»90s, Bartke wrote a grant application proposing to study the giant, growth - hormone - flooded
mouse as an example of accelerated
aging.
A
mouse engineered to have Alzheimer's disease and a gradual reduction
in levels of the brain enzyme BACE1 stopped forming plaques (arrows
in the first panel)
as it
aged.
The researchers then decided to see what would happen if they boosted sirtuin levels
in normal
mice as they
aged.
Furthermore, examination of
aged mice showed dramatically reduced levels of Cbf - beta
in bone marrow cells,
as compared to younger
mice.
In addition to colitis, these
mice also developed a form of colon cancer (known
as colitis - associated cancer)
as they
aged.
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.
As a result, they have less than half of the fat tissue found
in normal,
aged mice.
By examining first pregnancies
in aged mice, the team showed that, for
mice as for humans, the risk of complications increases with
age.
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.»
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.
As mice and humans
age, levels of that protein circulating
in the blood rise, Alzheimer researcher Tony Wyss - Coray at Stanford University and colleagues found.
The authors also found abnormalities
in the subthalamic nucleus occur earlier than
in other brain regions, and that subthalamic nucleus nerve cells progressively degenerate
as the
mice age, mirroring the human pathology of Huntington's disease.
Walford's new research is based on the fact that
in mice and humans, the immune system malfunctions during
aging, losing the ability to distinguish between healthy cells and invasive pathogens such
as bacteria and viruses.
In one group of
mice, he and his colleagues dosed their mothers with a synthetic compound that simulates a mild viral infection during late pregnancy; when their offspring hit early puberty at about 6 weeks of
age, the young
mice were exposed to unpredictable stress, such
as being restrained, deprived of water, or given electric foot shocks.
As the
mice aged, they became hyperactive, anxious, and antisocial,
in addition to having problems with movement that mirrored patient symptoms.
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.
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.
They noted a reduction
in the number of spines
as the
mice aged and their Alzheimer's disease progressed.
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.
The discovery
in mice could upend current notions about why people gain weight
as they
age, and could one day lead to more effective weight - loss medications.
Investigating
mouse models for biological for research The congress aims to promote the International Mouse Phenotyping Consortium (IMPC) mouse lines, importance of mouse phenotyping & clinical and drug discovery collaboration, to present progresses performed by IMPC with regards CRISPR editing genome, rare diseases, microbiota and ageing pipeline, as well as illustration of examples of scientific projects about «Animal models for human diseases» and recent developments in mouse models phenotyping ima
mouse models for biological for research The congress aims to promote the International
Mouse Phenotyping Consortium (IMPC) mouse lines, importance of mouse phenotyping & clinical and drug discovery collaboration, to present progresses performed by IMPC with regards CRISPR editing genome, rare diseases, microbiota and ageing pipeline, as well as illustration of examples of scientific projects about «Animal models for human diseases» and recent developments in mouse models phenotyping ima
Mouse Phenotyping Consortium (IMPC)
mouse lines, importance of mouse phenotyping & clinical and drug discovery collaboration, to present progresses performed by IMPC with regards CRISPR editing genome, rare diseases, microbiota and ageing pipeline, as well as illustration of examples of scientific projects about «Animal models for human diseases» and recent developments in mouse models phenotyping ima
mouse lines, importance of
mouse phenotyping & clinical and drug discovery collaboration, to present progresses performed by IMPC with regards CRISPR editing genome, rare diseases, microbiota and ageing pipeline, as well as illustration of examples of scientific projects about «Animal models for human diseases» and recent developments in mouse models phenotyping ima
mouse phenotyping & clinical and drug discovery collaboration, to present progresses performed by IMPC with regards CRISPR editing genome, rare diseases, microbiota and
ageing pipeline,
as well
as illustration of examples of scientific projects about «Animal models for human diseases» and recent developments
in mouse models phenotyping ima
mouse models phenotyping imaging.
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).
Hypothesis driven approaches to vaccinology can utilise the knowledge gained from mechanistic
mouse models and our molecular understanding of intrinsic defects to human cells.5 However, caution is required when extrapolating data from murine models,
as there are substantial differences between immune
ageing in mice and humans.6 Nevertheless, model systems and ex vivo analyses of molecular alterations
in aged human cells have identified multiple changes
in the vaccination response with
age and the
aged immune system
in general.
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.
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.
Angiotensin II receptor type 1 (Agtr1a): Lowering Agtr1a protein levels protects mitochondrial function and modestly extends life
in mice, though
as for many of these methods of somewhat slowing
aging there are probably many other changes to the operation of metabolism that are
as yet unexplored.
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.
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 happenstanc
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 happenstanc
as a part of any
aging or longevity study, and the longevity of these
mice is a fortunate happenstance.
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.
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).
Similarly, using SmartCube ® technology we identified distinct behavioral changes
as early
as 6 - 7 weeks of
age in SOD1
mice and 12 - 14 weeks for PFN1
mice.
Treatment with AFF 1 or vehicle control was initiated
in mThy1 -
AS mice at
age 3 mo, when early sensorimotor deficits first appear — similar to the target population for the first rollout of the human vaccine.
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.
(8) Imputation of these results specifically to the animals»
age - related, low - BubR1 - driven rise
in p16Ink4a - expressing senescent cells was, however, limited: limited by the very nature of so - called «accelerated
aging» models such
as BubR1H / H, (9) and limited by the lifelong, global absence of p16Ink4a expression
in the backcrossed
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 mic
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 mic
in similar -
aged WT
mice.
Currently, Everon is optimizing several lead compounds: small molecules and biologics that have already demonstrated a rejuvenation effect
in aging animals,
as measured by a lowered
mouse FI (similar FI has recently been accepted by FDA
as a measure of
aging in the ongoing Metformin human trial).
This early hint that
age - related changes
in EP2 action
in microglia might be promoting some of the neuropathological features implicated
in Alzheimer's was borne out
in subsequent experiments for which Andreasson's team used
mice genetically predisposed to get the
mouse equivalent of Alzheimer's,
as well
as otherwise normal
mice into whose brains the scientists injected either A-beta or a control solution.
Gontier and colleagues found that
as mice age, Tet2 levels
in the hippocampus decline,
as do the epigenetic tags Tet2 makes on DNA.
Oisín's platform 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.
Higher serum levels of pro-inflammatory factors such
as interleukin - 6 and tumor necrosis factor are found
in aged mice.
It should be noted, however, that while a study on senescent cell ablation
in genetically normal
mice would provide at least some evidence on the effect of senescent cells (and their ablation) on promoting cancer, even such a study would likely show less effect than could be anticipated
in a large mammal model, since even normally -
aging mice rarely suffer metastatic disease to the extent of
aging humans,
as sheer primary tumor volume is generally sufficient to be fatal to
mice.
Methods: R6 / 2 CAG 240 (peak training at 11 weeks of
age), zQ175 knock
in (KI) HET (peak training at 27 weeks of
age) and BAC HD (peak training at 48 weeks of
age),
as well
as respective
age - matched wild type (WT) control
mice, were trained on the peak interval task (20 s interval)
in which response rates during unreinforced peak trials were examined.
As the investigators note, the rapid
age - related arterial stiffening and cardiac arrhythmias that appear to be at cause for the majority of deaths
in BubR1H / H
mice were not attenuated by ablating p16Ink4a - expressing senescent cells — but these tissues had little burden of such cells, so this finding reinforces the conclusion that the multiple
aging phenotypes arrested
in these
mice when senescent cells were ablated is attributable specifically to the removal of their baleful influence on local tissues.
The success of the treatment
in older
mice, which corresponded to late adulthood
in humans, is particularly important,
as this would be the
age that would be targeted were this method ever to be used therapeutically
in people.
The congress aims to promote the International
Mouse Phenotyping Consortium (IMPC) mouse lines, importance of mouse phenotyping & clinical and drug discovery collaboration, to present progresses performed by IMPC with regards CRISPR editing genome, rare diseases, microbiota and ageing pipeline, as well as illustration of examples of scientific projects about «Animal models for human diseases» and recent developments in mouse models phenotyping ima
Mouse Phenotyping Consortium (IMPC)
mouse lines, importance of mouse phenotyping & clinical and drug discovery collaboration, to present progresses performed by IMPC with regards CRISPR editing genome, rare diseases, microbiota and ageing pipeline, as well as illustration of examples of scientific projects about «Animal models for human diseases» and recent developments in mouse models phenotyping ima
mouse lines, importance of
mouse phenotyping & clinical and drug discovery collaboration, to present progresses performed by IMPC with regards CRISPR editing genome, rare diseases, microbiota and ageing pipeline, as well as illustration of examples of scientific projects about «Animal models for human diseases» and recent developments in mouse models phenotyping ima
mouse phenotyping & clinical and drug discovery collaboration, to present progresses performed by IMPC with regards CRISPR editing genome, rare diseases, microbiota and
ageing pipeline,
as well
as illustration of examples of scientific projects about «Animal models for human diseases» and recent developments
in mouse models phenotyping ima
mouse models phenotyping imaging.