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).
Not exact matches
«
Aging - induced inflammatory activation of microglia could
only be prevented when
mice were fed a low - fat diet
in combination with limited caloric intake,» says Eggen.
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.
Although of course there are a number of caveats since
mice can be cured from cancer at higher rates, they don't suffer from some of our diseases, they are sensitive to being handled (if grabbing them can shorten their lifespan through stress, the
mouse version of standard human medical care may do the same), so I guess that increases
in maximum lifespan are indeed the
only reliable indicator that an intervention is impacting
age - related mortality.
In an operant test R6 / 2 transgenic
mice (240 - CAG repeats, B6 congenic background) were less able to acquire lever pressing than control animals at an
age where motor function is
only mildly affected (from 9 weeks), with this deficit being both more pronounced and detected earlier (from 5 weeks) where reinforcement was not solely contingent on responding.
Interestingly, we detected upregulation of p16 and p15
in Polycomb - null skin epithelial stem cells
in young
mice where it is normally detected
only in aged animals.
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.
[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.
In the climbing task, 90 % of the 110 CAG mice stopped climbing by 6 weeks of age in contrast to the 240 CAG repeat cohort in which only 55 % had stopped climbing by 8 weeks of ag
In the climbing task, 90 % of the 110 CAG
mice stopped climbing by 6 weeks of
age in contrast to the 240 CAG repeat cohort in which only 55 % had stopped climbing by 8 weeks of ag
in contrast to the 240 CAG repeat cohort
in which only 55 % had stopped climbing by 8 weeks of ag
in which
only 55 % had stopped climbing by 8 weeks of
age.
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.
Although we can not rule out that exercise might also increase hippocampal progranulin
in 2 - to 3 - month - old Grn + / −
mice, there is no data that an increase of this magnitude (
only 10 — 15 %) restricted to hippocampus would be sufficient to produce functional improvement, and the fact that the effect is not sustained even until ∼ 4 months of
age makes it highly unlikely to yield any sustained benefit after onset of functional changes between 6 and 12 months.
The findings thus provide preliminary evidence for an interaction between
age and exercise
in modulating progranulin expression, with effects of exercise
only in very young
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.
A reanalysis of genes tied to life span
in mice reveals
only a select few affect
aging.
In one Japanese study, for instance, researchers were
only able to change the baseline stress characteristics of germ - free
mice until nine weeks of
age.