Articles tagged with Mouse Models
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A transgenic mouse model was created with the K141N mutation in HSPB8 to study Chinese Charcot-Marie-Tooth disease type 2L. The mice exhibited decreased muscle strength and impaired motor coordination, but not sensory disturbance. Pathological analysis revealed reduced myelinated fiber density and axonal damage.
Researchers have developed a new mouse model that accurately replicates the progression of Alzheimer's disease in humans. The models are characterized by early accumulation of Abeta peptides and cognitive dysfunction similar to human patients.
Researchers develop genetically engineered mice with inherited brachyury gene change to study chordoma development. The mice will be made available to scientists through The Jackson Laboratory's repository.
Researchers found that repeated hUCB MNC injections produced greater neuroprotection in mice modeled with MPS III B, preserving hippocampal structure and reducing microglial activation. The treatment also showed promise in modulating anxiety and inflammation.
A study published in PLOS Pathogens found that rosiglitazone, a known diabetes drug, can prevent brain damage in mice with cerebral malaria and increase brain-derived neurotropic factor (BDNF) levels in humans. The findings suggest that this approved drug may have protective mechanisms against long-term cognitive impairments.
Researchers at CNIO have identified two novel treatments for psoriasis, one targeting S100A9 and the other inhibiting miR-21, which show promise in reducing side effects. These discoveries offer new hope for patients suffering from this chronic disease.
Researchers developed a new mouse model of atopic dermatitis, revealing mast cells and Stat5 play critical roles in the disease. The study identified potential targets for eczema treatment based on links to human disease.
Research reveals Metabotropic Glutamate Receptor 5 (mGluR5) as a potential therapeutic target for treating movement disorders like Huntington's disease. The study found that blocking mGluR5 improved motor behaviors in a mouse model, suggesting its potential for treating Parkinson's disease as well.
Researchers have developed a nonsense suppression drug that can restore function in mice with aniridia, a progressive disease affecting the eyes and brain. The treatment, ataluren, was administered topically to postnatal aniridia mice and successfully reversed eye deformations and restored vision.
Researchers identified a fungal surface protein that promotes host cell invasion in mucormycosis, while others found that melanocytes from light-skinned humans secrete a molecule promoting angiogenesis. These findings could lead to new treatments and biomarkers for diseases associated with increased vascularization.
Research using a mouse model of Loeys-Dietz syndrome reveals that enhanced TGF-beta signaling contributes to the development of aortic aneurysms. Treatment with Angiotensin II type 1 receptor antagonists shows promise in ameliorating aortic aneurysm progression.
Researchers found that rapamycin treatment increases survival and prevents disease progression in a mouse model of Leigh syndrome. The drug delays neurological symptoms, reduces brain inflammation, and extends lifespans by more than triple.
Researchers found that hemin injection caused labored breathing, lung injury and rapid death in sickle mice, but not in control mice. Hemopexin was an effective treatment against hemin-induced lung injury.
Researchers develop mouse model of hereditary spastic paraplegia linked to changes in endoplasmic reticulum structure associated with REEP1 mutations, which impair ER function. The new model provides insight into how ER morphology affects axon loss in HSP.
Researchers have identified a molecular signature in human tissue samples from women who experienced premature birth. A combinatory treatment strategy involving rapamycin and progesterone effectively prevented preterm birth in mice model, suggesting potential for reducing incidence in high-risk women.
Researchers found that AD mouse models with neurodegeneration have 25% more copper in their amyloid plaques than those without, suggesting altered copper regulation may contribute to neurotoxicity. Iron levels were also increased, particularly in the ferric state, and may serve as a biomarker for early-stage AD.
Researchers at Whitehead Institute created mouse models of two neurodegenerative diseases that are fatal in humans. The highly accurate reproduction of disease pathology seen with these models should advance the study of prion diseases, including Creutzfeldt-Jakob disease and fatal familial insomnia.
Researchers have identified a modification to the protein eIF2alpha linked to Alzheimer's-like conditions, which may lead to decreased protein synthesis and impaired long-term memories. Abnormal levels of phosphorylation were found in AD model mice and postmortem human patients, highlighting potential therapeutic targets.
Researchers discovered a protein linked to cognitive impairments in Angelman syndrome, a condition characterized by autism, intellectual disability, and motor abnormalities. The study found that reducing the expression of this protein improved cognitive function in Angelman syndrome model mice.
A large new resource of mouse lines has been created to study human diseases, revealing new functions for well-known genes and unexpected associations with traits like body weight. The project provides a wealth of freely available clinical and biological information to aid in the development of new therapies.
Researchers have discovered a biomarker that can track Huntington's disease progression using electrical activity in brain waves. The study found abnormalities in specific frequency bands prior to the onset of symptoms, suggesting a potential early indicator of the disease.
Researchers at Stanford University School of Medicine developed a mouse model that accurately mimics the course of Duchenne muscular dystrophy in humans. The study demonstrates a molecular basis for the cardiac defect and provides evidence for a potential treatment to prolong heart function.
RG3039 demonstrates benefits in two SMA mouse models, extending survival and improving motor unit function. The drug also positively modifies motor unit pathologies and dysfunction, suggesting potential therapeutic benefit for SMA patients.
Researchers developed a mouse model to study MPNST, identifying genes FOXR2 and NF1/PTEN pathways involved in its development. The study aims to repurpose existing therapeutics for MPNST treatment and explore new targeting strategies.
Researchers created a new mouse model to study the development of type 2 diabetes, using middle-aged mice fed fatty food until old age. The study confirmed that inflammation in pancreatic islets leads to the disease, while DPP-4 inhibitors maintain good insulin production and prevent inflammation.
Researchers found that a Bortezomib/Vorinostat combination therapy reactivated virus-induced cell lysis and induced PEL cell death, increasing the lifespan of mice with PEL tumors. This treatment combination could potentially be beneficial for immunocompromised patients with KSHV-associated malignancies.
Researchers characterized SUDEP in a mouse model of Dravet Syndrome and found that a prolonged slowing of the heart beat preceded SUDEP. Treatment with certain drugs reduced the incidence of SUDEP, suggesting mortality results from seizure-related parasympathetic hyperactivity.
Diabetic patients are more likely to die from a heart attack, and high levels of ox-CaMKII may be the key. Researchers found that reducing CamKII oxidation could help treat diabetic patients with cardiovascular disease.
Studies show that mouse models do not reflect the human genomic response to inflammatory injury, including major burns and trauma. Despite similar responses among humans, mouse models exhibit limited correlation with gene expression changes.
Researchers found higher uropathogenic E. coli reservoirs in post-menopausal women's bladders compared to pre-menopause, which can lead to UTIs. Estrogen supplementation reduced these reservoirs dramatically, highlighting a potential new approach to prevent or treat UTIs in this population.
A study published in American Journal of Pathology found that tamoxifen can counteract some pathologic features in a mouse model of Duchenne muscular dystrophy. Tamoxifen improved muscle force, diaphragm and cardiac structure, reducing fibrosis by up to 50%.
Researchers have identified a genetic variant associated with an increased risk of autoimmune diseases like type 1 diabetes. In a mouse model study, turning off the PTPN22 gene reduced the risk of autoimmune diabetes and increased regulatory T cells.
Researchers developed a mouse model of obesity where the proopiomelanocortin gene can be turned on and off to study the impact of chronic weight gain. Turning the gene back on after prolonged obesity reduced its effectiveness.
Researchers have created a genetic mouse model to study primary ovarian insufficiency (POI), a condition affecting one in a hundred women. The model replicates the effects of POI on ovaries and fertility, providing new insights into its causes and potential treatments.
Researchers developed a mouse model of Fukuyama's muscular dystrophy that accurately replicates human disease pathology. The study found that removing the fukutin gene at different stages of development led to varying degrees of muscle impairment.
Investigators found that low oxygen levels increase SMN2 exon 7 skipping, reducing survival motor neuron protein levels. Higher oxygen treatment improved motor function and reduced disease severity in a mouse model of severe SMA.
Researchers from Case Western Reserve University School of Medicine developed a mouse model that mimics the N48K mutation in Usher III, leading to understanding of how deafness occurs. This new model enables exploration of prospective therapeutics to rescue mutant protein localization and hearing.
Researchers created a mouse model to study the role of AEG-1 in hepatocellular carcinoma, demonstrating its acceleration of disease progression and angiogenesis. The study paves the way for novel therapies targeting AEG-1.
A team of researchers at UC Davis has identified several proteins as diagnostic biomarkers and potential therapeutic targets for kidney cancer. The study used metabolomics techniques to analyze chemicals in urine and serum samples from mice implanted with human kidney cancer cells.
A new study has identified the Nkx2.5 gene as the first gene linked to congenital asplenia, a rare condition where babies are born without a spleen and are at risk of fatal infections. The discovery raises hopes for genetic prenatal screening to alert parents to potential issues.
Researchers developed a mouse model of delirium, finding that systemic inflammation triggers short-term memory disturbance, which is reversed by treatment with donepezil. The study reconciles two long-standing hypotheses, shedding light on the condition's causes and potential treatments.
Researchers discovered that radiation treatment inhibits monocyte entry into the optic nerve head, preventing neuronal damage in a mouse model of glaucoma. This breakthrough sheds light on a potential prevention strategy for glaucoma, which is one of the leading causes of vision loss and blindness worldwide.
A Nationwide Children's Hospital study found that muscle regeneration may create an ideal environment for rhabdomyosarcoma to arise. The research uses mouse models of muscular dystrophy to investigate the growth of eRMS, a fast-growing and highly malignant tumor subtype.
Researchers have discovered a new mouse model for Multiple Sclerosis, using diabetic mice to replicate the disease's relapsing and remitting symptoms. This breakthrough may lead to the development of more effective treatments that turn temporary recovery into permanent repair.
Researchers at the University of Alabama, Birmingham have found that mutations in primary cilia can disrupt the functioning of the melanin concentrating hormone receptor, leading to increased appetite and weight gain. This discovery sheds light on the potential link between ciliopathies, such as Bardet-Biedl syndrome, and obesity.
Researchers at UGA have developed the world's first transgenic mouse model with Hirano bodies, which may play a protective role in the progression of neurodegenerative diseases such as Alzheimer's. The new model will allow scientists to study the impact of Hirano bodies on cell survival and disease progression.
Researchers created a mouse model that displays remarkably similar symptoms and behavior as children and adults on the autism spectrum. The animals responded well to an FDA-approved drug prescribed to treat repetitive behaviors often associated with the disease.
Researchers at Harvard Medical School found that modulating Irs2 levels can slow HD progression by reducing nerve cell damage and increasing lifespan. Decreasing Irs2 levels attenuated symptoms of the disease.
Researchers have discovered blood proteins associated with early lung cancer development in mice and humans, offering a promising avenue for a non-invasive blood test. The study found distinct protein signatures in mouse models and human patients, which could aid in diagnosis and monitoring of the disease.
Researchers have developed a genetically engineered mouse model to study Lafora disease, revealing the role of malin-laforin complex in glycogen synthesis and neuronal degeneration. The study provides evidence for abnormal sugar accumulation leading to neuronal deterioration and death.
Researchers have developed a mouse model for Charcot-Marie-Tooth disease and discovered a potential therapy using HDAC6 inhibitors, which halted damage to nerves and reversed symptoms. This treatment could offer new hope for an incurable disease affecting approximately one in 2,500 individuals.
New data from two independent research groups provides hope that a therapeutic approach can be developed to treat SMA. Prolactin treatment increases SMN levels, improves muscle movement, and enhances survival in mouse models of severe SMA.
A study by Lukas Van Oudenhove and colleagues found that a fat solution to the stomach attenuates behavioral and nerve cell responses to sad emotion in humans. This discovery has implications for treating disorders such as obesity, eating disorders, and depression. Additionally, two independent research groups have generated new data o...
Researchers developed a new mouse model to test cancer drugs by simulating gene inhibition, preventing rapid cell division in cancer cells while leaving healthy cells unaffected. The study published in Nature Communications validates the preclinical relevance and predictive value of the inducible RNAi-based mouse model.
Researchers found that glia support neurons and provide energy substrates necessary for function. Re-expression of MeCP2 solely in astrocytes rescues lifespan, breathing, anxiety, and locomotor activities associated with Rett Syndrome in mouse models.
Researchers developed a mouse model of Familial Hemiplegic Migraine type 2, showing increased susceptibility to cortical spreading depression. The study suggests that episodic disruptions in the excitation-inhibition balance may underlie migraine vulnerability.
Researchers from Ruhr-University Bochum discover that mutations in the CCDC66 gene are responsible for retinitis pigmentosa, a leading cause of inherited blindness. They also develop a genetic test for diagnosis and predictively breeding in dogs, with potential implications for human patients.
Researchers have developed a genetically humanized mouse model for hepatitis C, enabling the testing of molecules that block the virus's entry into cells. The new model has the potential to serve as a critical role in prioritizing drug and vaccine candidates.
Researchers replicated inflammatory gene changes of human kidney progression from mild to severe diabetic nephropathy using a mouse model. The study could lead to new understanding and potential treatments for diabetic nephropathy, the leading cause of kidney failure.
Pitt researchers created a mouse model of major depressive disorder (MDD) using a rare genetic mutation. The model exhibits alterations in brain anatomy, gene expression, behavior, and increased infant mortality, supporting the role of the genetic variant in MDD development.