Not exact matches
The team found neonatal
mice with the mutations had
normal - appearing skin, and the dry itchy skin of dermatitis did not develop until the
mice were a few months
old, the equivalent of a young adult in human years.
These
mice performed better than their
normal counterparts on learning tests well into
old age, and their brains did not exhibit the decline in neurogenesis typically seen in aged
mice.
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.
Older modified male
mice metabolised sugar faster than
normal mice and females, suggesting that SIRT6 might extend life by protecting against metabolic disorders such as diabetes.
«The
mice also did not seem to gain weight when they got
older, like
normal mice do.
Normal mice reach sexual maturity at about 30 days
old, but the leptin - treated
mice blossomed about 3 days earlier, Flier says.
However, when the researchers knocked out SIRT1 in endothelial cells of 10 - month -
old mice, then put them on a four - week treadmill running program, they found that the exercise did not produce the same gains seen in
normal 10 - month -
old mice on the same training plan.
They found that at 6 months of age, these
mice had reduced capillary density and could run only half as far as
normal 6 - month -
old mice.
If an
old mouse was p16 - deficient, it regrew pancreatic cells and cured itself like a
normal young
mouse.
The
older mice fed a diet containing extra amounts of vitamin E, the equivalent to about 200 IU / day consumed by humans — about 10 times the Recommended Daily Allowance but well below the upper limit — were far more resistant to the bacteria than the
older mice that had a
normal amount of vitamin E in their diet.
Raised in a germ - free environment, and then given a transplant of gut microbes from a four - day -
old normal mouse, these
mouse were still able to resist Salmonella infection without any help from their immune system — but only when they had received a dose of added Clostridium first.
However, by the time these
mice reached adulthood, around 8 months
old, the level of photoreceptor cells in these knockout
mice was less than half the
normal level.
They found that the samples from the
older normal mice had the most diversity of their gut microbes, including Clostridia and Bacteroides bacteria not seen in the younger
mice that were still getting their nutrition entirely from mother's milk.
But when the researchers added bacteria from 16 - day -
old normal mice, the amount of C. rodentium in the guts of surviving
mice went down.
Left: The gut of a
mouse that received a transplant of microbes from the gut of four - day -
old normal mice, and then was exposed to Salmonella, while the other received a transplant of the four - day -
old mouse microbes along with added Clostridia bacteria, before being exposed to Salmonella.
Nunez, Kim, Sakamoto and their colleagues carried out a careful series of experiments using both newborn and adult germ - free
mice, and samples of gut microbes taken from the feces of 4 - day -
old, 12 - day -
old and 16 - day -
old normal 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.
Based upon activity in multiple CNS toxicity assays, we identified an exceptionally potent, orally active, neurotrophic molecule called J147 that facilitates memory in
normal rodents, and prevents the loss of synaptic proteins and cognitive decline when administered to three - month -
old APP / swePS1ΔE9
mice for seven months [7].