Articles tagged with Mouse Models
Researchers at the University of California, Irvine have developed a new genetically engineered mouse model that mimics the most common form of late-onset Alzheimer's disease. The model, which embodies the remaining 95% of cases, holds promise for understanding causes of the disease and developing new treatments.
Research using three mouse models of neurodevelopmental disorders found distinct basal metabolism patterns, with varying energy expenditure and fat utilization. The studies suggest all three models may exhibit mitochondrial dysfunction, highlighting the need for personalized treatments and diagnostic methods.
A study published in International Journal of Molecular Sciences suggests a link between corticotropin-releasing hormone (CRH) and increased expression of mast cells in the nasal cavity, exacerbating allergic reactions. The research offers promising therapeutic potential with CRHR1 inhibitors and SCF neutralizing antibodies.
Researchers designed and tested 32 inhibitors targeting the SARS-CoV-2 main protease, a key viral protein required for replication. The study found six compounds with high potency to protect cells from infection, offering promise for the development of orally available anti-SARS-CoV-2 drugs.
Researchers used a mouse cachexia model to investigate myocardial damage in tumor-bearing mice, finding suppressed oxidative phosphorylation and glycolysis. The study validates the model for studying cancer-derived myocardial impairment, revealing various changes associated with cancer cachexia.
A new mouse model created by researchers at the University of Bonn reveals that GPI anchor deficiencies, a group of rare diseases, are caused by impaired transmission of stimuli at brain synapses. The mice exhibited cognitive deficits, altered social behavior, and increased susceptibility to epilepsy, mirroring human symptoms.
Researchers found that deleting FATP4 increases cone photoreceptor survival and visual function nearly 10-fold in mouse models of Leber congenital amaurosis. This discovery establishes FATP4 as a promising therapeutic target to preserve daytime color vision in patients with RPE65 gene mutations.
A repurposed mouse model has been shown to develop symptoms of severe COVID-19 and milder disease, including loss of the sense of smell. The study found that convalescent plasma protected the mice against lethal disease, suggesting a promising tool for understanding COVID-19 and developing new treatments.
Researchers identify RTL1 gene as likely culprit behind temple and Kagami-Ogata syndromes, associated with muscle symptoms in models of both conditions. The study suggests that RTL1 plays a critical role in fetal muscle development and is essential for maintaining placental fetal capillaries.
A new mouse model shows that injecting synthetic assembled tau protein causes tau accumulation in wild-type mice, spreading to connected regions. This study establishes that tau assembly does not require mutation or overexpression.
Researchers demonstrate that one dose of RNA-targeting CRISPR-Cas9 gene therapy can nearly completely reverse symptoms in a mouse model of myotonic dystrophy, reducing toxic RNA buildup by over 50%. This approach holds promise for treating other genetic diseases caused by repetitive RNA buildup.
Researchers at RIKEN IMS discovered that a combination of gut bacteria worsens multiple sclerosis symptoms in a mouse model. Two specific bacteria, OTU002 and Lactobacillus reuteri, enhance immune cell activity that attacks the brain and spinal cord.
Scientists developed a new automated movement-tracking system, LocoMouse, to capture fine details of locomotion in mice. The study identified highly-detailed 'locomotor signatures' for two mouse models, providing a roadmap for linking neurological and locomotor deficits.
Researchers developed an injectable clotting agent called HAPPI that slows internal bleeding by 97 percent in mice. The agent can be stored at room temperature and reconstituted before injection, making it a potential game-changer for trauma care.
A team of researchers used a mouse model to test the best therapeutic option for a type of relapse sarcoma. The study found that two treatment regimens administered to a patient with lung metastasis helped extend their disease-free period to 46 months.
A novel mouse model shows that contained and persistent yet non-pathogenic Mtb infection reduces tuberculosis disease burden after re-exposure. The study highlights the importance of innate immune responses in protecting against the disease.
Researchers found persistent DNA damage in placentas of mice with cohesin mutations, leading to senescence and pro-inflammatory cytokines affecting embryonic growth. Targeting cytokine signaling may be a way to protect the health of the placenta and promote healthy pregnancies.
Researchers have developed a groundbreaking mouse model of human prion disease, demonstrating spontaneous formation of disease-relevant prion protein assemblies in mice with only human forms of the prion protein. This discovery is expected to provide valuable insights into human disease and inform the development of therapies.
Heidelberg researchers demonstrate that restoring VEGFD levels can preserve dendritic arborisation and reduce brain damage after a stroke. A treatment using recombinant VEGFD and nose drops achieved similar results in mouse models.
Researchers found that Huntington's model mice bred to lack IL-6 exhibited exacerbated symptoms compared to those with IL-6. Gene expression differences revealed reduced synaptic signaling pathways in IL-6 deficient mice.
The National Institutes of Health has renewed funding for UC Davis's Mutant Mouse Resource and Research Center, providing $6.7 million over five years. The center will acquire new mouse strains and develop novel models to support biomedical researchers.
Researchers used the homozygous G608G BAC-transgenic progeria mouse model to study degenerative joint diseases. Treatment combinations with pravastatin and zoledronic acid significantly improved bone mechanical properties and cartilage structural parameters.
Researchers at CNIC have created a novel mouse model that enables the direct analysis of protein mechanical function. The model, based on titin and HaloTag-TEV genetic cassette, allows for controlled disruption of protein mechanics to study cellular responses.
Kidney stone disease is associated with impaired lipid metabolism and downregulation of fatty acid-binding protein 4 (FABP) 4. FABP4 plays a key role in kidney stone formation and may be a therapeutic target for prevention.
A new therapy called antisense oligonucleotide (ASOs) has shown dramatic effects in a mouse model of SCN8A-related encephalopathy, reducing mRNA expression by half and increasing lifespan by four-fold.
The new mouse model accurately reflects human genetic and immune system characteristics, enabling researchers to test new treatments. It can reverse damage to the small intestine once it has developed, providing a vital tool for improving quality of life for people with celiac disease.
A team at Columbia University's Mailman School of Public Health has developed a new method that accurately predicts human disease outcomes based on gene expression in individuals infected with Ebola. The model uses machine learning and was tested on a data set collected from Ebola patients in western Africa, confirming its accuracy.
A new mutation in the mt-Cyb gene of a mouse model for GRACILE syndrome drastically speeds up disease progression. The discovery provides a valuable tool for studying mitochondrial diseases and their function.
Researchers at Universitat Pompeu Fabra developed a non-invasive method of stimulating the vagus nerve in mice, leading to improved memory. The study used electrostimulation in the ear, which stimulated areas of the brain important for memory, resulting in better performance in object recognition memory.
Researchers found that cromolyn sodium delayed the development of ALS symptoms in mice with a genetic mutation causing the disease. The treatment also protected neurons from degeneration and reduced inflammation by targeting mast cells.
A study analyzing data from four types of mouse Alzheimer's models found consistent changes in cell number and gene expression throughout the disease stages. The research provides new targets for intervention and therapy, highlighting the immune system's involvement in early stages of Alzheimer's.
Researchers have discovered that a gene mutation in the chloride channel causes hyperaldosteronism, leading to abnormally high blood pressure and kidney damage. The study used a mouse model to investigate the pathological mechanisms of the disease, providing insights into the effects of an open chloride channel on aldosterone production.
Researchers used an optimized AAV9 vector to deliver the galactosylceramidase gene to a mouse model of Krabbe disease, improving clinical symptoms and prolonging median survival. The treated mice lived up to 150 days, compared to 41 days for untreated mice.
A new study created lab mice by implanting embryos from laboratory animals into wild mice, resulting in a model that accurately predicts human response to drugs. This novel approach has the potential to improve translational research value for immunology, potentially preventing failed clinical trials.
Researchers developed a new mouse model called 'wildling,' which acquired microbes and pathogens from wild mice while maintaining laboratory genetics. The study found that wildlings mirrored human immune responses, were stable in their microbiota, and predicted human immune responses with accuracy.
A machine learning algorithm identified altered pupil diameter fluctuations in mouse models of autism spectrum disorders, allowing early detection of developmental disorders. The algorithm distinguished Rett syndrome patients from controls based on heart rate fluctuations, suggesting a potential biomarker for early detection.
Researchers developed a mouse model that recapitulates Parkinson's disease's progression, showing how misfolded protein α-synuclein spreads from the gut to the brain. The study supports Braak's hypothesis and suggests potential therapeutic targets.
Scientists have developed a new gene-targeted approach to study chronic wasting disease in mice, allowing for the detection of distinct prion strain properties in deer and elk. This breakthrough enables researchers to better understand the ability of prions to transmit disease between species.
A new protein, CAPON, has been linked to the connection between amyloid-β plaques and tau pathology in Alzheimer's disease. Accumulation of CAPON increases AD-related pathology, while deficiency reduces symptoms. The study uses novel mouse models to explore this link.
Researchers have created a novel mouse model of psoriatic arthritis (PsA) by infecting non-obese diabetic mice with an adenoviral vector expressing single-chain IL-23, resulting in symptoms similar to human disease. This breakthrough model can be used to test and optimize PsA therapies.
A mouse model of autism has shown that exercise eliminates excess connections between neurons characteristic of ASD. After one month of voluntary running, behavioral differences disappeared and structural brain differences were reduced.
A study published in JNeurosci reports that dysfunctional neurons in the hippocampus of adult mice modeling dementia can be repaired and reconnected to distant parts of the brain. The findings suggest potential new treatments for cognitive decline in the elderly.
Researchers found that mirabegron increases cholesterol synthesis in mouse models of atherosclerosis, leading to accelerated plaque growth and increased cardiovascular risk. The changes were linked to thermogenic fat breakdown induced by mirabegron treatment, raising concerns for patients with LDL receptor mutations.
Researchers have identified two fast-acting compounds that kill parasite-supporting bacteria after a single dose in mouse models of filarial diseases, potentially eradicating the condition. The standard-of-care treatment is limited by its duration and availability to pregnant women and children.
A new study found that a slow-growing variant form of Lyme bacteria causes severe symptoms and resists standard single-antibiotic treatment. A three-antibiotic cocktail eradicated the infection in mice, offering a potential solution for patients with persistent Lyme disease symptoms.
Researchers at University of Bath created a mouse model for Joubert Syndrome by deleting portions of the Talpid3 gene, reproducing physical abnormalities and progressive ataxia in mice. The study aims to accelerate research into the disease and develop new treatments.
Researchers at University of Toledo have developed a mouse model that spontaneously develops type I diabetes and its complications, allowing for study of disease progression. The breakthrough has the potential to reshape how type I diabetes is studied and may lead to new treatments or a cure.
A study found that cannabinoid receptor type-1 is involved in memory problems associated with Down syndrome. Inhibiting CB1 receptors improved memory and synaptic plasticity in mouse models.
Researchers have created a novel mouse model that demonstrates how epigenetic changes can negatively impact a key gene involved in neurodevelopment and behavior. The study provides direct causal evidence linking this gene to autism spectrum disorder (ASD)-like behavior.
Researchers identified a potential pathway for creating effective treatments against CMV, a common viral infection that can be deadly for stem cell transplant patients. A serum containing antibodies matched to the infecting viral strain prevented CMV reactivation after periods of dormancy.
A study using murine models found that a neutralizing monoclonal antibody, ZIKV-195, protects mice from Zika virus infection. The antibody targets and cross-links envelope proteins critical for viral membrane fusion.
Researchers created a viable mouse model of Hirschsprung's disease to study its development and progression. The new model revealed that mucin-producing goblet cells may be a target for preventative treatment and that reduced expression of GFRa1 contributes to susceptibility to the disease.
A new mouse model has revealed the crucial role of PARL in maintaining mitochondrial respiratory chain function and structural integrity. The study found that mice lacking PARL display symptoms reminiscent of Leigh syndrome, highlighting the importance of understanding the protein's mechanisms in neurodegenerative diseases.
A new study reveals that incorporating genetic diversity into a mouse model of Alzheimer's disease improves translatability, enabling more accurate predictions and potential treatments. The Resilience-Alzheimer's Disease Consortium has created a genetically diverse panel of mice with Alzheimer's mutations.
A study published in JCI Insight found that a specific subset of immune B cells, CD19+IgM+, can delay the onset of type 1 diabetes in mice. This discovery opens up new possibilities for developing therapies targeting this disease subtype.
Researchers found that administering Lactobacillus reuteri reversed social deficits in ASD mouse models through the vagus nerve and oxytocin-dopamine reward system. The study suggests a novel approach to treating neurological disorders by modulating specific microbes in the gut.
A new AI model has been developed to translate mouse model data to human disease conditions, increasing the accuracy of extrapolation by up to 50%. The model, known as Found In Translation (FIT), has been tested on 28 different human diseases and uncovered novel disease-associated genes.
Scientists at Newcastle University have identified a gene editing method to stop kidney damage in patients with Joubert syndrome, a genetic condition causing brain and kidney issues. The 'exon-skipping' technique may lead to personalized therapies for inherited kidney diseases.
Researchers have developed a mouse model expressing human tau protein to study the effects of repetitive brain injury on cognitive function, motor dysfunction and white matter damage. The study found that repetitive concussive injuries resulted in chronic disruptions in white matter and associated neuroinflammation.
Researchers developed a transgenic mouse model of Parkinson's disease, replicating PD-like motor symptoms and α-synuclein aggregation. The study suggests that stabilizing normal αS tetramers may prevent or delay PD onset.