Articles tagged with Mouse Models
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.
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 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.
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.
A study published in PNAS has reversed symptoms of Smith-Magenis syndrome in mice by reactivating the RAI1 gene. This breakthrough may lead to new treatments for this neurodevelopmental disorder. Researchers used optogenetic stimulation to restore social interaction deficits, providing hope for improved patient outcomes.
Researchers found that papaverine reduces tumor oxygen consumption and hypoxia in mouse models, making tumors more sensitive to radiation. This suggests repurposing papaverine to enhance radiation therapy effectiveness.
Gonorrhea is a rapidly worsening public health threat with over 550,000 new cases reported in 2017 and global yearly incidence estimated at 106.1 million cases. Researchers warn that animal models, like mouse models, may not accurately reflect the infection's severity or human immune responses.
Remnants of the extracellular matrix promote inflammation and airway remodeling in asthma. Accumulation of PGP may explain why LTA4H inhibitors have failed in clinical trials.
A new study shows that a single injection of AAVB1-GAA gene therapy prolonged survival and improved enzyme activity in a mouse model of Pompe disease. The therapy also targeted the respiratory system, improving ventilatory measures.
Researchers can now access eight new mouse models carrying genetic mutations found in patients with late-onset Alzheimer's disease. These models express variants at genetic loci associated with the disease but not yet proven to be causative, offering a significant advancement in AD research.
Research shows that a pharmacological strategy can alleviate multiple behavioral and cellular deficiencies in a mouse model of fragile X syndrome. Treatment with GSK6A or a similar compound could be a viable strategy for addressing cognitive and behavioral problems in fragile X syndrome.
A team of researchers has developed a mouse model of myotonic dystrophy type 1, revealing multiple mechanisms beyond alternative splicing. The study found a clear association between specific signaling pathways and muscle loss, as well as the upregulation of protein AMPK-alpha and the reduction of PDGFR-beta signaling activity.
A new rabbit model with clinical similarity to human patients has been developed for Duchenne muscular dystrophy (DMD) research. The model exhibits signs of muscular dystrophy, including impaired physical activity and muscle loss, making it a promising tool for advancing DMD research and developing novel therapies.
A new mouse study suggests that the widely used antimicrobial ingredient triclosan may have adverse effects on colonic inflammation and colon cancer. Researchers found that triclosan altered gut microbiota, increased inflammation, and spurred disease development in mice.
Researchers found that TDP-43 and DISC1 protein clusters disrupt dendritic local translation, leading to abnormal cell function and behavior. The study provides a new insight into the molecular mechanisms underlying psychiatric symptoms in neurodegenerative diseases.
Changes in neuron size have been linked to the progression of motor neurone disease, with vulnerable neurons increasing in size before symptoms appear. This could lead to new strategies for slowing or halting nerve cell death and improving treatment options.
Researchers found that crizotinib enhances radiosensitivity of tumors and inhibits growth of cultured tumor cells from NF2 patients. A novel mouse model mimicking NF2-associated hearing loss was also created to study the molecular pathway contributing to tumor progression and radiation-induced hearing loss.
Scientists have identified the OTUD7A gene as a key contributor to the clinical characteristics of 15q13.3 microdeletion syndrome, a complex neurological condition. The study found that mice deficient in the gene Otud7a have fewer dendritic spines, which may be related to the neurological deficits observed in patients.
Researchers found that restricting food availability to a set schedule improved motor activity and sleep quality in mice with Huntington's disease. These findings suggest that eating on a strict schedule could improve quality of life for patients with neurodegenerative diseases.
Researchers developed a mouse model where the FXN gene defect causing Friedreich’s ataxia can be turned on or off, revealing that many early symptoms are reversible. The study found that reducing frataxin levels led to symptoms similar to those seen in humans with the disease, which disappeared when frataxin levels returned to normal.
Scientists have discovered a novel mechanism that prevents glioblastoma development through the modulation of EFGR expression by RanBP6. The study reveals that silencing of RanBP6 promotes glioma growth by upregulating EGFR expression, while reconstitution of RanBP6 leads to reduction in tumor growth.
Scientists develop modified CRISPR-Cas9 technique that alters gene activity without cutting DNA, reversing diseases in mice models. The technique uses adeno-associated viruses to introduce genetic manipulation machinery to cells, promoting expression of target genes without introducing mutations.
Researchers created an animal model that closely replicates the human form of Alzheimer's disease, including pathological tau protein and amyloid plaques. This breakthrough allows for testing of new therapies targeting both pathologies.
Researchers at Karolinska Institutet discovered that Alagille Syndrome is caused by malformations of the bile ducts, leading to serious liver and heart problems. The study provides new insights into the disease and opens up possibilities for targeted therapies.
A single infusion of wildtype hematopoietic stem and progenitor cells into a mouse model of Friedreich's ataxia restored normal cellular functions, halted cellular damage, and improved mitochondrial function. This breakthrough suggests a potential therapeutic approach for the currently incurable disease.
Researchers used gene therapy to stop the immune response that causes multiple sclerosis in mouse models, producing near-complete remission. The treatment combined a brain-protein gene with an existing medication, showing significant potential for treating multiple sclerosis and other autoimmune disorders.
Researchers from Instituto de Medicina Molecular created a chimera virus that can test molecules to treat cancers caused by human herpes virus infection in mice models of disease. This finding preserves the functionality of LANA, a protein vital for Kaposi virus maintenance, allowing new cancer treatments to be developed.
Scientists identified a compound, FR, that provides long-lasting airway relaxation and prevents hyperreactivity in mouse models of asthma. The locally administered compound also blocks aspects of airway remodeling without causing cardiovascular side effects.
Researchers at Vanderbilt University Medical Center have developed a small molecule compound that works like the dimmer switch in an electrical circuit, relieving symptoms of Rett syndrome in mice. The study provides further evidence that a drug may be possible to treat this rare neurodevelopmental disorder in females.
The Jackson Laboratory will investigate a new mouse model for amyotrophic lateral sclerosis (ALS) with a $3.2 million federal research grant. The study aims to link genetic mutations in the mouse models to human ALS or other neuromuscular diseases.
A new study suggests that the small molecule LM22A-4 can improve spatial memory and motor skill defects in Rett syndrome mice by enhancing synaptic plasticity in the hippocampus. The treatment also shows promise for improving breathing problems associated with the disease.
Researchers found that increasing serotonergic activity in a mouse model of autism improved social behavior and reduced abnormal brain activity. The study suggests that serotonin may be potentially therapeutic for discrete ASD symptoms.
A new mouse model has been created to investigate kidney cancer, allowing researchers to develop better treatments. The model reveals that gene mutations in the primary cilium contribute to renal cell carcinoma's progression.
Researchers have created a promising mouse model for the devastating genetic disorder NGLY1 deficiency. The double-deletion mice survive and exhibit symptoms analogous to humans with the condition, making them useful for testing potential therapies.
Researchers at JAX will study mouse models of inherited RPE-driven disease to identify potential molecular pathways for druggable targets. Their goal is to prevent, delay onset or decrease the severity of age-related macular degeneration and other heritable retinal diseases.