Articles tagged with Mouse Models
Researchers at the University of Florida have discovered a protein that stimulates fat metabolism when stressed, leading to weight gain. The study found betatrophin, a previously touted diabetes treatment, has a new role in regulating body fat.
Researchers used genetically-modified mice to study hereditary deafness caused by mitochondrial dysfunction. Reducing enzyme activity in mice showed promise for preventing or delaying deafness, according to new research.
Researchers have developed a new mouse model for spinal muscular atrophy that responds to therapy, allowing for post-symptomatic treatment and potentially improving outcomes for patients. The treatment, an antisense oligonucleotide, restores motor unit function in the muscles even after symptoms have begun.
Researchers develop novel mouse model for Leber hereditary optic neuropathy and demonstrate successful gene therapy in improving visual function. The approach could aid therapy development for various mitochondrial diseases, with a clinical trial currently underway.
Research identifies a key trouble spot in the brain that contributes to intellectual disability in Down syndrome, shedding light on disrupted brain networks. The study suggests therapies targeting these networks may be beneficial for future treatments.
Researchers develop new approach to treating Rett syndrome by extending lifespan and improving behavioral symptoms in mouse models. The treatment targets PTP1B, an enzyme with abnormal levels in the disorder, restoring BDNF signaling and promoting neural growth.
Researchers at Case Western Reserve University used stereomicroscopy to create detailed 3D images of mouse models of IBD, revealing distinct patterns related to health and disease. The findings suggest two mouse models most closely resembling human forms of the illness.
Researchers at Mayo Clinic developed a mouse model exhibiting neuropathological and behavioral features associated with C9ORF72 mutation. The study suggests a link between the repeat expansion in C9ORF72 and TDP-43 pathology, potentially leading to therapeutic agents targeting RNA foci and c9RAN proteins.
Researchers at IDIBELL have created new mouse models for studying neurofibromatosis type 1, a rare genetic disorder. The models, which reproduce human tumor characteristics, enable the prediction of tumor development and treatment decisions.
Researchers found that M-MDSCs can inhibit both T cell and B cell proliferation, leading to improved symptoms in arthritic mice. The study suggests a potential role for M-MDSCs in treating autoimmune diseases like arthritis.
Researchers have developed a long-lasting, glucose-responsive insulin derivative called Ins-PBA-F, which self-activates when blood sugar levels rise. Tests on mouse models show that one injection works for up to 14 hours, automatically lowering blood sugar levels.
Researchers used a century-old drug, suramin, to reverse environmental and genetic autism-like symptoms in mice. The approach blocked the cellular danger response signal, allowing cells to restore normal communication and reversing ASD symptoms.
A mouse study identified a malfunctioning neural circuit as the root of motor impairments seen in autism, where abnormal synaptic pruning and Purkinje cell function contribute to motor learning deficits. The findings may shed light on the intense world syndrome phenomenon in autism.
Researchers found that Lactobacillus species in the guts of mouse models correlated with reduced lupus symptoms, while Clostridia increased. Probiotics containing Lactobacillus may help alleviate lupus flares, suggesting a potential new treatment approach.
Researchers developed an AAV-mediated gene therapy approach to correct hyperbilirubinemia in a mouse model of Crigler-Najjar syndrome type 1. The treatment achieved significant, long-lasting reductions in bilirubin levels, with 50-70% reductions maintained throughout the study.
A new mouse model closely resembles human non-alcoholic steatohepatitis (NASH) and demonstrates that interfering with key inflammatory proteins inhibits disease development and cancer progression. The study uses a genetically modified mouse strain to show the effectiveness of anti-inflammatory compounds in preventing NASH.
Recent studies reanalyze gene expression patterns in mouse models, finding greater similarities with human disease conditions, contrary to a 2013 study that suggested poor correlation. The new research highlights the potential of mouse models for studying human disorders and developing treatments.
Scientists discovered consistent alterations in integrative processing of the insular cortex across autism mouse models, with a disturbed balance between excitation and inhibition. Pharmacological interventions, such as Diazepam, restored sensory integration capacity and reduced stereotypic behaviors.
Researchers studied rat and mouse models of focal cerebral ischemia to develop high-quality rodent models of stroke. They found optimal methods for middle cerebral artery occlusion in rats (0.40-0.45 mm, 18-20 mm thread insertion length) and mice (0.15-0.18 mm, 9-11 mm thread insertion length).
Two studies using different mouse models confirm that comorbid Alzheimer's disease and cerebrovascular disease significantly worsen learning and memory outcomes in mice. Researchers say the findings have potential implications for patients with both disorders, who account for approximately 40% of Alzheimer's cases.
A mouse model of endometriosis has been developed that produces lesions similar to those found in humans. The study suggests that macrophages present in shed endometrium contribute to the development of endometriotic lesions, providing new insights into the disease.
Researchers at Allen Institute for Brain Science will map connectivity patterns across whole brain in mouse models of Alzheimer's disease. The goal is to understand pathways through which the disease spreads and develop effective treatments.
Neuroscientists at SRI International have found that a form of baclofen works better at treating narcolepsy than the best drug currently available when tested in mice. The research team also presents a mouse model of narcolepsy that mimics the human disorder, allowing for more precise control of hypocretin/orexin neuron loss and potent...
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.