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.
Supporting cell characteristics in long - deafened
aged mouse ears.
Now, new research from the laboratory of Vaijayanti P. Kale (National Centre for Cell Science, Pune, Maharashtra, India) has described a fascinating new approach to return lost functionality to
aged mouse HSCs: the transfer of microvesicles (MVs) containing positive regulators of autophagy derived from young mesenchymal stem cells (MSCs)[6].
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.
«And at the higher dose, we saw a rescue of the neural stem cell pool in
aged mice.»
Similar research since has found what may be the genetic signatures of Norwegian Viking
Age mice in modern populations on the Azores, an island chain more than 900 miles west of Portugal.
Even more striking, the gene - expression pattern in the hippocampi of THC - treated
aged mice was radically different from that of untreated elderly mice.
Partial reprogramming of cells within prematurely
aging mice's bodies extended the rodents» average life span from 18 weeks to 24 weeks, researchers report December 15 in Cell.
Now,
ageing mice have been given a new lease of life after being injected with a drug that jump - starts their mitochondria.
Normal mice saw benefits, too: Muscles and pancreas cells healed better in middle -
aged mice that got rejuvenation treatments than in mice that did not.
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.
A genetic switch linked to memory impairment in
ageing mice has been flipped back on, restoring failing brains to a more youthful state.
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.
Additionally, the team found that induced lifelong overexpression of Nampt, an enzyme important in making NAD, prevented the natural decline in NAD and partially preserved exercise capacity in
aged mice.
The GDF11 protein commonly found in the blood of young mice (the same protein that enhanced neurogenesis in
aged mice) and placed in individual older mice was thought to have the same reversal effect on hypertrophy; however, more recent research suggests another molecule besides GDF11 may be at work.
«Caloric restriction in combination with low - fat diet helps protect
aging mouse brains: Low - fat diet plus limited caloric intake prevented aging - induced inflammatory activation of microglia; exercise was significantly less effective than caloric restriction in preventing these changes.»
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.
Similar to humans,
the aged mice exhibited enlarged hearts, a general thickening of the heart wall and a reduced efficiency in the hearts ability to pump blood.
Furthermore, examination of
aged mice showed dramatically reduced levels of Cbf - beta in bone marrow cells, as compared to younger mice.
They gave
aging mice (engineered to have deficient immune systems that would not adversely react to human plasma) infusions of the three types of plasma every fourth day for two weeks.
However, when the researchers used drugs or mouse mutations that reduced the number of monocytes or removed TNF, they were able to restore antibacterial immunity in
aged mice.
View our related Science in the Classroom annotated research paper on rejuvenation of
the aging mouse brain.
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.
The team examined tissues in mice for cellular stress following acute SD, and they also looked for cellular stress in
aging mice.
There is increased ER stress in the pancreas of
aged mice.
As a result, they have less than half of the fat tissue found in normal,
aged mice.
In
aged mice with diabetes (represented on the right), Tregs are overexpressed in fat tissue and trigger insulin resistance.
By examining first pregnancies in
aged mice, the team showed that, for mice as for humans, the risk of complications increases with age.
Viruses were used to deliver Arc to middle
age mice, after the critical window had closed.
Overexpressing a single gene called Arc rejuvenates the visual cortex of middle -
age mice, making them as plastic as younger mice.
Now the researchers have studied the effects of shortened telomeres on
aging mice.
«High folic acid intake in
aged mice causes a lowered immune response.»
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.
Indeed, the research team reported that
aged mice did not exhibit signs of cartilage regeneration after treatment with UBX0101 injections.
«The first question was whether RbAp48is downregulated in
aged mice,» said lead author Elias Pavlopoulos, PhD, associate research scientist in neuroscience at CUMC.
The researchers also did functional MRI (fMRI) studies of the mice with inhibited RbAp48 and found a selective effect in the DG, similar to that seen in fMRI studies of
aged mice, monkeys, and humans.
This effect of RbAp48 inhibition on the DG was accompanied by defects in molecular mechanisms similar to those found in
aged mice.
Next, Abadir and colleagues compared the effects of different concentrations of losartan and valsartan on young diabetic and
aged mice during the proliferation / remodeling phase of wound healing, which involves the regrowth of normal tissue.
The current study reports neurogenesis (neuron creation) occurred in the spinal cords of both adult and aged (over one - year old) mice of both sexes, although the response was much weaker in
the aged mice, Dr. Zhang said.
Development of diet - induced fatty liver disease in
the aging mouse is suppressed by brief daily exposure to low - magnitude mechanical signals
The researchers tested their theory by orally administering a drug that inhibits DNA - PK and found that, in addition to preventing weight gain in the mice, the inhibitor drug boosted mitochondrial content in skeletal muscle, increased aerobic fitness in obese and middle
aged mice, and reduced the incidence of obesity and type - 2 diabetes.
Vascular and neurogenic rejuvenation of
the aging mouse brain by young systemic factors.
At 10 months of
age the mouse models were found have no amyloid plaque deposits at all.
A Combination of Fast - Clearance Nandrolone Plus Low - intensity Aerobic Exercise Improves RBC Indices in Anemic
Aging Mice
Loss of responsiveness to melatonin in
the aging mouse suprachiasmatic nucleus.
In today's paper, the team reported what happened when the researchers turned on that killswitch in middle -
aged mice, effectively scrubbing clean the mice of senescent cells.
This research has been suggested before using cell cultures and in artificially
aged mice, but this is the first time that a naturally - aging model has been used.
Outflow of cerebrospinal fluid is lymphatic - specific and reduced in
aged mice Steven Proulx, ETH Zurich
p38 MAPK signaling underlies a cell - autonomous loss of stem cell self - renewal in skeletal muscle of
aged mice.