Articles tagged with Mouse Models
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.
Scientists have developed a new mouse model with a healthy immune system to study the Zika virus. The model allows researchers to investigate the immune response to Zika, which could lead to advances in vaccine development and treatment strategies.
Researchers propose a new therapy for Gaucher disease by blocking the molecule C5aR1, which drives inflammation and organ damage. The treatment may offer fewer risks and lower costs than current therapies.
A team of researchers has discovered a novel approach to treating juvenile Batten disease by activating a protein called TFEB, which stimulates the cell to produce more lysosomes and degrade cellular waste. This breakthrough may lead to improved neurological symptoms in patients with the condition.
Research from the University of British Columbia found that a vitamin A deficiency in the womb or early infancy can increase production of amyloid beta and lead to cognitive impairments. Providing supplements after birth may help slow the degenerative brain disease.
Researchers developed a new mouse model that faithfully reproduces the pathologies of COPD and CF, revealing two key pathways: oxidative stress and protease-antiprotease imbalance. The model shows promise for developing new medication therapies.
New research identifies physiological changes in the body that could explain why older mothers are more likely to experience complicated births. The study found that maternal age influences the structure of the uterus, leading to impaired muscle contraction properties, reduced sensitivity to oxytocin, and altered hormonal signals.
A new mouse model has revealed the role of CCN6 protein in developing metaplastic breast cancer, a rare and aggressive subtype of triple-negative breast cancer. The study identified potential genes to target with therapeutics, offering hope for better treatment options for patients.
Researchers developed a mouse model to assess early tissue responses to biomaterials, including bioactive glass. The model's feasibility and reliability have been demonstrated using various biomaterials, enabling the design of novel biomaterials for regenerative medicine.
Researchers have discovered a potential treatment for Prader-Willi syndrome (PWS), a rare genetic disorder affecting children, by activating silenced genes. The NIH-funded study found that two drugs, UNC0638 and UNC0642, improved survival and growth outcomes in mice with PWS.
Scientists found that female mice are more susceptible to vaginal Zika virus infection during a specific stage of their reproductive cycle. The study suggests that sex hormones play a role in allowing the virus to establish itself in the reproductive tract and spread beyond it.
Researchers confirm live Zika virus infects reproductive tract, replicates and causes disease in mouse models. Hormonal injection timing affects vulnerability to infection, with diestrus-infected mice showing no signs of disease despite viral persistence.
Researchers at the Forsyth Institute have defined the immune-regulatory mechanisms of Sjögren's syndrome, revealing how PD-L1 and PD-1 proteins interact to suppress protective immunity. The study found that inhibiting this pathway accelerates autoimmune responses and disease development.
A team of scientists has developed a mouse model that closely mimics fetal brain abnormalities caused by the Zika virus, revealing abnormal blood vessel formation and a leaky blood-brain barrier. This finding highlights the need to understand all the effects of Zika infection if successful therapies are to be developed.
Researchers have developed a new mouse model that can be used to study the Zika virus and its effects on the body. The model, which employs mice with functioning immune systems, has been shown to develop symptoms of neurological disease after infection, providing valuable insights into potential treatments.
Researchers have developed two new mouse models of amyotrophic lateral sclerosis (ALS) that exhibit protein clumping and display clinical features seen in patients. The models may help scientists better understand the disease and develop new treatments.
A pediatric otolaryngologist is developing a mouse model to identify the most effective treatment for respiratory papillomatosis, a rare condition that can cause chronic hoarseness and breathing problems in children. The goal is to provide personalized medicine and reduce the need for frequent surgeries.
Researchers from Ben-Gurion University of the Negev discovered a novel molecular mechanism that could lead to new therapies for ALS. They found that endogenous multifunctional protein macrophage migration inhibitory factor (MIF) acts as a chaperone for misfolded SOD1 proteins, which accumulate and cause cell death in ALS patients.
Researchers from University of Eastern Finland discovered that retinal changes can be detected earlier than brain changes in CNS diseases. Functional abnormalities were found in three genetically engineered mouse models of human CNS diseases, suggesting eye examinations could be used as a noninvasive screening tool.
The grant will accelerate the creation of high-priority mouse models for Charcot-Marie-Tooth disease and other peripheral neuropathies. Researchers aim to investigate disease mechanisms and develop treatments, which currently have no cures or effective treatments.
Researchers developed a mouse model that mimics human Alzheimer's disease, showing that beta-amyloid accumulation is insufficient to trigger tau clumping alone. The study suggests combination therapy targeting both processes may be effective in preventing the disease.
A study published in Cell Reports has found that inhibiting the enzyme cdk4 can prevent and reverse the initial stage of Non Alcoholic Fatty Liver Disease (NAFLD). Researchers at Cincinnati Children's Hospital Medical Center used two FDA-approved drugs to inhibit cdk4, significantly reducing hepatic steatosis in mouse models.
Researchers at UC Santa Barbara have discovered a possible first therapy for Mucolipidosis IV by extending their findings from fruit flies to a mouse model. Bone marrow transplantation significantly delayed the onset of motor deficits in MLIV mice, preventing the amplification process that causes neurodegeneration and blindness.
Research from Baylor College of Medicine found that Notch activation promotes metastasis in prostate cancer by upregulating FoxC2, a molecule important for metastatic potential. The study used a mouse model with prostate-specific loss-of-function Pten to demonstrate the role of Notch in prostate cancer progression.
Scientists at Hong Kong University of Science and Technology discover that interleukin-33 (IL-33) rescues contextual memory deficits and reduces beta-amyloid peptide deposition in AD mouse models, suggesting a new therapeutic intervention.
Researchers have discovered that caspase 12 does not act as a dominant-negative regulator of caspase-1 activation and inflammasomes. This finding challenges a stubborn dogma in the field and opens up new avenues for studying caspase 12's role in physiological processes.
Researchers found that endocannabinoids quiet neurons in the orbitofrontal cortex, leading to an over-reliance on habit. The study suggests a new therapeutic target for OCD and addictions: treating the brain's endocannabinoid system to restore goal-directed action.
Researchers have established mouse models of Zika virus transmission from a pregnant mouse to her fetus, demonstrating viral invasion and damage to the placenta. The studies reveal that Zika virus can cause congenital problems, including fetal death, by breaching the placental barrier.
A study published in PLOS Neglected Tropical Diseases describes a suitable small animal model for testing ZIKV interventions. The A129 mouse model accumulates virus in the brain and other tissues, exhibiting symptoms similar to those in humans.