Articles tagged with Mouse Models
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.
Researchers developed a transgenic mouse model of the rare neurodegenerative disorder HDL2 to study its pathogenesis. The study found overlapping polyQ-mediated mechanisms with Huntington's disease and identified a novel expanded polyQ protein driving disease progression in HDL2 mice.
A new study reveals that rapamycin can reverse cardiac muscle damage in a mouse model of LEOPARD syndrome, a rare congenital heart disease. The research demonstrates the importance of targeted therapies in managing congenital diseases and offers a potential new treatment option for patients with LEOPARD syndrome.
Researchers at University of South Florida found that spirulina supplementation delayed motor symptoms and disease progression in a mouse model of ALS. The study suggests a dual antioxidant and anti-inflammatory effect on motor neurons, offering potential clinical benefits for ALS patients.
Overexpression of PGC-1α significantly improves neurological function in HD-model transgenic mice by reducing htt protein aggregation and oxidative stress. This discovery may lead to therapies targeting PGC-1α function for treating Huntington's disease and related disorders.
Joslin researchers found that brain cholesterol synthesis decreases in mouse models of diabetes, affecting nerve function and potentially leading to increased appetite and weight gain. The study suggests a link between diabetes and altered brain function, including changes in Alzheimer's disease risk and diabetic neuropathy.
Researchers at Joslin Diabetes Center discovered that diabetes can reduce brain cholesterol synthesis, which could impact brain function and increase the risk of Alzheimer's disease. This finding has broad implications for people with diabetes and may also play a role in diabetic neuropathy.
A new mouse model created by Japanese scientists confirms the link between mutated beta-synuclein protein and neurodegeneration in diseases like Parkinson's and Alzheimer's. The discovery establishes B-synuclein as a potential target for developing new therapies.
Researchers identify hyperactive c-Met protein as key player in ADPKD cyst growth, leading to potential therapeutic target. Pharmacological inhibition of c-Met decreases mTOR activity and blocks cyst formation in mouse model.
A single stimulatory molecule has been found to sustain human insulin-producing cell replication in a mouse model of diabetes, indicating potential treatment options for the condition.
Researchers at Biogen Idec Inc. have found that targeting the TIM-1 protein may be effective in treating asthma. The study used a humanized mouse model to show that an antibody binding to a specific region of TIM-1 reduced inflammation and airway hyperresponsiveness.
Researchers at Columbia University Medical Center found a genetic variant causing disrupted communication between brain regions, leading to working memory deficits and increasing the risk of schizophrenia. The study used a mouse model with a 22q11 deletion mutation, which showed impaired neural activity and behavior in cognitive tasks.
Researchers have identified CD99 as a potential new drug target for Ewing sarcoma. A novel type of cellular senescence has also been found to suppress prostate tumorigenesis. Additionally, the protein USAG-1 has been linked to the development of Alport syndrome, suggesting a promising therapeutic approach.
Researchers have identified a potential new set of targets to improve the efficiency of pancreatic islet transplantation. The study found that treatment with an antibody targeting HMGB1 prevented early pancreatic islet loss and inhibited IFN-gamma production by NKT cells and Gr-1+CD11b+ cells.
Researchers found that taking nonsteroidal anti-inflammatory drugs (NSAIDs) like ibuprofen or naproxen can prevent the early sign of Alzheimer's disease in mice. However, these same drugs do not reverse existing neuronal cell cycle events in affected animals.
Researchers at Caltech have shown that a highly specific intrabody can stall the development of Huntington's disease in various mouse models. The treatment successfully attenuated symptoms and increased life span by targeting an amino-acid sequence unique to the mutant huntingtin protein.
Researchers have developed a new mouse model of amyotrophic lateral sclerosis (ALS) that closely replicates human symptoms, including progressive paralysis and muscle loss. The genetically engineered mice also exhibit damage to motor neurons and protein clumps, similar to human ALS pathology.
A team of researchers led by Dr. Alon Monsonego has created a humanized mouse model that responds specifically to an A-beta-peptide vaccine, reducing plaque and inflammation in the brain. The study provides a basis for developing individualized immunotherapeutic approaches to Alzheimer's disease.
Researchers have identified a new mechanism underlying sex-specific gene expression in mice, with PPAR-alpha repressing genes involved in immunity and steroid production. The study also found that this repression is mediated by sumoylation, a process only occurring in female mice, and suggests potential new approaches to prevent estrog...
Scientists have developed a new mouse model of X-linked nephrogenic diabetes insipidus, a severe kidney disease. The model shows that selective EP4 receptor agonists alleviate the symptoms of the disease, suggesting these compounds as potential therapeutics.
Researchers created a mouse model with low kalirin levels that developed schizophrenia symptoms as an adolescent, mimicking human delayed onset. The study suggests stimulating kalirin activity could help alleviate cognitive symptoms, offering new treatment direction.
Research reveals that blood-derived macrophages with interleukin-10 expression have an anti-inflammatory effect on spinal cord injuries. This finding suggests that these cells may contribute to the recovery process after injury.
Researchers have identified protein Nox4 as crucial for hemangioma growth and found a potent inhibitor fulvene-5 to substantially inhibit its growth. This discovery suggests targeting Nox4 using fulvene derivatives may attenuate hemangioma growth.
A team of scientists at Children's Hospital of Pittsburgh UPMC has discovered an enzyme crucial for maintaining a robust immune system into old age. The study found that the novel mouse model has a thymus that remains intact throughout its life.
A new mouse model has been developed to understand the cause of progressive hearing loss, opening up avenues for treatment. The study found that a genetic mutation in microRNA seed region influences sensory hair cell production, leading to impaired hearing.
Scientists have created a mouse model of Wolf-Hirschorn Syndrome, a genetic disorder characterized by physical abnormalities and developmental delays. The model, which mimics the disease's effects on cardiac valves and facial structures, offers a valuable tool for researchers studying human development and disease.
A humanized mouse infected with HIV has enabled researchers to test antiviral protection against AIDS. The study shows that pre-exposure treatment and post-exposure treatment can prevent both vaginal and rectal transmission of the virus.
A team of Columbia University researchers has identified a new investigational therapy for bladder cancer, inhibiting the mTOR signaling pathway with rapamycin. The discovery demonstrates that p53 and PTEN tumor suppressor genes are inactivated in invasive bladder cancer.