They found that the mice developed earlier and more severe
disease than mice that had normal Tob1 expression in all cells including CD4 +.
An accelerated progression may show up in clinical trials in human males, who live longer with
the disease than mice.
Not exact matches
«We don't know if the observed reversibility of the
disease symptoms as observed in the
mouse,» he says, «exists in humans who have a much longer period of pre - and post-natal brain development
than mice — months and years in humans, weeks in
mice.»
Among
mice that had antibodies, i.e., during antibody - enhanced infection, the researchers found that the addition of saliva extract caused more severe
disease than virus alone.
The behavioral tests used here modeled one dimension of the
disease — an inability to experience pleasure from normal activities — but not others, such as stress and anxiety, and probably tap into different brain mechanisms in
mice than in humans, he says.
With no more
than a change in diet, laboratory agouti
mice (left) were prompted to give birth to young (right) that differed markedly in appearance and
disease susceptibility.
When the
mice were just four months old — well before they showed symptoms of the
disease — their synaptic mitochondria had accumulated approximately five times more amyloid protein
than nonsynaptic mitochondria had.
«What we found was, if we block mGluR5, which is the glutamate receptor we're interested in, the
mice become hyper locomotive so they become able to move better
than wild type
mice suggesting glutamate receptors might be a good target for treating movement disorders such as Parkinson's
disease.
A dye used for more
than a century to stain autopsied brain tissue can prevent the devastating effects of Huntington's
disease in
mice, new research shows.
The
mice, described in this month's issue of Nature Genetics, also may provide a quick way to screen potential drugs for the
disease, a disabling condition that afflicts more
than a third of U.S. women over the age of 60.
The vaccine slowed the progression of prion
disease in the remaining 70 % of the experimental
mice, allowing them to live longer
than control
mice, which did not receive the vaccine and died within about 200 days following infection.
Once the microglia were mobilized in
mouse models of Alzheimer's
disease, the researchers observed a more
than 60 percent reduction in amyloid beta in the brain.
Furthermore, more
than 75 % of
mice infected with virus bearing the normal protein developed severe corneal autoimmune
disease, whereas fewer
than 20 % of
mice infected with mutant virus did, and their symptoms were barely detectable.
The new study — published October 18, 2016 in the journal Molecular Psychiatry — combined genetic analysis of more
than 9,000 human psychiatric patients with brain imaging, electrophysiology, and pharmacological experiments in mutant
mice to suggest that mutations in the gene DIXDC1 may act as a general risk factor for psychiatric
disease by interfering with the way the brain regulates connections between neurons.
Half of the
mice studied, belonging to a genetic line that suffers a form of Crohn's
disease were more affected
than the remaining half of
mice, which belong to a healthy
mouse line.
«The
disease progression was much faster in the crossbred
mice than in the standard
mice,» Connor said.
«The dog has a retina very similar to ours, much more so
than mice, so when you want to bring a visual therapy to the clinic, you want to first show that it works in a large animal model of the
disease,» said lead researcher Ehud Isacoff, professor of molecular and cell biology at UC Berkeley.
Mice bred to carry a gene variant found in a third of ALS patients have a faster disease progression and die sooner than mice with the standard genetic model of the disease, according to Penn State College of Medicine research
Mice bred to carry a gene variant found in a third of ALS patients have a faster
disease progression and die sooner
than mice with the standard genetic model of the disease, according to Penn State College of Medicine research
mice with the standard genetic model of the
disease, according to Penn State College of Medicine researchers.
With the risk for obesity - associated
diseases significantly higher for men
than women, researchers compared how
mice from each sex reacted to high - fat diets.
Lynch and the team, however, reasoned that a model that mirrored the slowly progressive nature of the
disease might be more valid
than the rapidly progressive
mouse models more commonly used.
His symptoms may come closer to mimicking the human
disease than most
mouse models of mental illness, because the gene involved has such a powerful effect.
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.
Experiments on
mice and on heart cells obtained from infants born with congenital heart
disease suggest that neuregulin 1, a human growth factor, can put infant heart cells on a path that mimics normal growth rather
than stalling out.
Using a model of Parkinson's
disease in which the toxin MPTP, made famous in book «The Case of the Frozen Addicts,» induces Parkinson's - like symptoms in humans and
mice, Dr. Smeyne showed that
mice infected with H1N1, even long after the initial infection, had more severe Parkinson's symptoms
than those who had not been infected with the flu.
SIGMAR1 deficiency accelerated
disease onset of SOD1 - ALS
mice by more
than 20 %.
Sinclair's lab is now working on developing what he calls a possible «supermouse» with elevated levels of NAMPT to see if it lives longer and is more
disease - resistant
than normal
mice.
The Weill Cornell researchers studied more
than 500 Crohn's
disease patients and found that those who carry a homozygous mutation in the CX3CR1 gene have a reduced gut antifungal response much like that seen in the
mice lacking CX3CR1 + phagocytes.
So when Drake and his colleagues measured the RNA levels — a direct link to how much of a gene is being produced — in the genes of 334
mice, he didn't expect to find more
than a few variations that might help explain why males and females have such different rates of cardiovascular
disease and diabetes or why they react differently to certain drugs.
In the study,
mice given a lethal dose of dengue virus less
than a week after receiving the protective DMAb were completely protected from lethal
disease — significantly more rapid
than vaccine - driven protection, which can take weeks to months to reach peak efficacy levels.
Specifically, rod - mediated inner retinal responses to dim light flashes were faster in
diseased mice than in their wild - type controls.
The
mice that were fed a calorie - restricted diet, mainly by a reduction in their carbohydrate intake, over a period of six months, had fewer
disease symptoms
than their normal - diet counterparts.
«Two is better
than one to improve brain function in Alzheimer's
disease mouse model.»
REG3G - deficient
mice also developed more severe alcoholic liver
disease than normal
mice.
Using two complementary approaches to reduce the deposits of amyloid - beta in the brain rather
than either approach alone improved spatial navigation and memory in a
mouse model of Alzheimer's
disease.
In
mice, the dose required for contraception was 10 times lower
than that required for treating Gaucher's
disease patients.
«We don't yet understand why
mice that develop severe inflammation express about 20 times higher levels of CD209a
than mice that do not develop severe
disease, and we don't yet know about the role of DC - SIGN in human schistosomiasis.
The researchers found that bacteria forming part of a cluster were more likely to be taken up by human cells and to survive in them
than the microbes without close relatives; the cluster strains also caused more severe
disease in
mice.
If sufficient 1,25 - dihydroxyvitamin D is produced, it may exert paracrine effects on surrounding T lymphocytes, thereby regulating the tissue - specific immune responses.10 Some support for this hypothesis comes from recent experiments showing that
mice fed diets high in vitamin D had significantly fewer clinical and pathological signs of EAE
than mice fed a vitamin D — deficient diet.37 Central nervous system levels of 1,25 - dihydroxyvitamin D, but not blood levels, were higher in supplemented
mice than in vitamin D — deficient
mice and correlated inversely with
disease severity.
To better understand this complex tissues and its functions — and the
diseases that affect it — a multicenter team led by researchers at the Broad Institute of MIT and Harvard and Massachusetts General Hospital has released a census of the cells that make up the lining of the small intestine, using gene expression profiles of more
than 53,000 individual cells from the
mouse gut or gut organoid models.
They do not appear to live any longer
than the rest of us, which is a caution for anyone extrapolating effects from
mice, and have a variety of medical issues associated with their form of dwarfism, but may be resistant to some forms of age - related
disease.
«Because scientists can selectively switch off genes in
mice, more will be learnt about human
disease from the
mouse genome
than from the human genome.
He notes that though ticks carry the
disease, its real reservoir in the wild is white - footed
mice, and their reproductive behavior is more susceptible to gene drive
than ticks.
The CRISPR / Cas technology applied to
mouse genetic engineering could quickly advance scientific understanding of
disease mechanisms by allowing researchers to ask complex questions and find answers much faster
than with traditional gene targeting approaches.
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.
There are lots of different HD
mice available, and because every case of HD is caused by the same basic genetic mutation, it may be that «our»
mice will turn out to be better
than those of other
diseases, at predicting success in human patients.
Results showed the first two groups didn't develop PCOS, unlike the
mice in the control group, whereas the test subjects with ovary ARs still contracted the
disease, albeit at a lower rate
than the normal
mice.
It creates customisable and high - scale
mouse models of human
disease or displaying an abnormality (KI, KO
mouse models) and it provides a complete phenotyping characterisation of the immune system by polychromatic and mass cytometry measuring more
than 50 simultaneous quantitative parameters in standardised conditions.
Vicky Robinson, of NC3Rs, which campaigns to reduce use of animals, said: «We can't assume a transgenic marmoset will be better for
disease research
than, for example, a transgenic
mouse.
These kind of
mice are an extraordinary resource for modeling human
disease; for instance, research has found that
mice that are genetically mutated to carry the BRCA1 gene (a human breast cancer gene) behave more similarly to human cancer patients
than those
mice who have had a tumor physically transplanted in.
«Still, as in humans,» says Reinholdt, «the success rate for Mendelian
disease gene discovery in the
mouse is only slightly better
than 50 percent.»