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
Sinclair thinks that these
mouse models
indicate that resveratrol may be effective in preventing
age - related diseases in humans, like cancer, heart disease and type 2 diabetes.
«Our results
indicate that the epigenetic modification we studied makes both
mice and humans more susceptible to obesity and with increasing
age increases their risk of developing a fatty liver,» said Anne Kammel, first author of the study.
The researchers then confirmed that the number of singly paired chromosomes — also called univalents — was higher in older
mouse and even human egg cells,
indicating that
age - related segregation errors could be tracked back to increased numbers of prematurely separated chromosome pairs.
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
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.
The research, which was performed in
mice,
indicates that a mother's health, even before conception, may influence the health of her fetus, and opens questions on how a mother's
age may influence placental development.
Significant differences between wt and XpdTTD / TTD but not between wt and XpdTTD / † XPCS
mice were observed at 9 and 18 mo of
age as
indicated by asterisks.
Intestinal inflammation in TNFΔARE
mice is clinically
indicated by weight loss and the disease fully develops by 8 weeks of
age.
We observed no significant effect of genotype for any of these genes (data not shown),
indicating that 7 - to 8 - month - old Grn − / −
mice have not yet developed the elevated levels of inflammatory cytokines found at older
ages (Filiano et al., 2013).
Additionally, we have previously detected decreased levels of respiratory chain proteins in the brains of
aged Polg mutator
mice from our colony, which would
indicate mtDNA damage (Hauser et al., 2014).
In contrast, no Slc6a14 − / − female with PyMT transgene developed tumours at 3 months of
age; however, at 4 months of
age, small tumour nodules became detectable (Figure 2B),
indicating a marked delay in mammary tumour development in PyMT - Tg
mice as a consequence of Slc6a14 deletion.
Analysis of escape latencies (Figure 3B) during training
indicated significant effects of
aging and, possibly, rapamycin, such that escape latencies were increased in
aged mice and were decreased by rapamycin treatment (P = 0.0021, P = 0.0548, and P = 0.2419 for
age, treatment, and
age / treatment interaction, respectively, 3 - way ANOVA with
age and treatment as between - subjects factors and training day as within - subjects factor).
For example, results of a
mouse study conducted by the National Institutes of Health (NIH) in collaboration with ChromaDex published in November 2014
indicated that NR was effective at restoring NAD + levels in mitochondria and rescuing phenotypes associated with a devastating accelerated
aging disease known as Cockayne Syndrome (CS).