Researchers created the largest metabolome analysis of the mouse brain, revealing distinct chemical conversions between brain regions. Aging mice showed significant metabolic differences in brain sections, with lipids playing a crucial role in changes to brain function.
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A recent study from the Okinawa Institute of Science and Technology Graduate University identified a crucial protein linked to increased appetite and obesity in mice. The researchers found that mice lacking this protein, XRN1, exhibited leptin resistance, leading to insatiable hunger and weight gain.
A recent study suggests that targeting alpha-synuclein protein in Parkinson's disease may not be sufficient to cure most patients. Instead, resolving brain inflammation caused by dysfunctional interferon-beta receptor signaling may hold the key to developing more effective treatments.
Researchers have developed a novel mouse model that accurately replicates the pathological propagation of tau protein isoforms in Alzheimer's disease, corticobasal degeneration, and Pick's disease. The model shows endogenous expression of both 3R and 4R tau, which accumulates in brain regions characteristic of each disease.
A study by Purdue University researchers has discovered a way to use gene therapy to turn glial brain cells into neurons, restoring visual function. This process is more efficient and less damaging than stem cell therapy, offering new hope for patients who have lost vision or motor skills after a stroke.
Researchers at Tokyo University of Science discover that vicarious social defeat can cause psychological stress in mice, leading to depression and decreased neurogenesis. The study sheds light on the pathophysiology of depression and may lead to the development of novel antidepressants.
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Researchers at RIKEN Cluster for Pioneering Research have found that Kleefstra syndrome, a genetic disorder leading to intellectual disability, can be reversed after birth. Postnatal treatment with artificially induced GLP production resulted in improved brain and behavioral symptoms.
Researchers at St. Jude Children's Research Hospital found that the tumor suppressor gene PTEN controls rhabdomyosarcoma cell identity and that enhancing PAX7 expression can maintain tumor cell existence, providing a potential treatment target for rhabdomyosarcoma.
A study by Cincinnati Children's Hospital Medical Center reveals that minor cells with mutations in the DDX41 gene can trigger a subset of inherited MDS cases. The research suggests that targeting these cells could lead to new treatment options for patients.
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A new approach called an immunobiological algorithm provides a comprehensive assessment of how a patient's immune system will react to tissue from each potential living donor. This method outperforms current HLA testing in identifying the best potential living donor, which could lead to improved organ transplant outcomes.
A new study from Salk Institute researchers found that a critical threshold of miR-218 levels determines the development of ALS in animal models. The study sheds light on the complex control of gene expression and its implications for treating neurological disorders.
A study published in Scientific Reports describes the putative molecular regulators of reductive stress — a microRNA network. The researchers identified a subset of miRNAs that appeared to be direct and dose-dependent targets of Nrf2, and thus putative regulators of reductive stress.
Researchers at St. Jude Children's Research Hospital have developed a more accurate laboratory model for studying retinoblastoma, a rare pediatric eye cancer. The models closely mimic the biology of patient tumors and provide an important resource for studying the earliest stages of the disease as well as screening new therapies.
Researchers identified two proteins, HMW1 and HMW2, that stimulate protective immunity against diverse NTHi strains. Immunization with these proteins provides protection against bacterial colonization by other strains, highlighting the vaccine potential for a nontypeable Haemophilus influenzae vaccine.
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Scientists discovered impaired leptin transport to the brain via LepR receptors leads to pre-diabetic state and exhausted insulin secretion. Reintroducing leptin restores pancreatic function-promoting action, suggesting a crucial brain role in type 2 diabetes management.
Researchers found that mice can make fine visual discriminations between slightly different lines, suggesting a more complex decision-making process than previously thought. The study's findings highlight the importance of considering non-perceptual biases in understanding animal behavior and decision-making strategies.
Researchers used genetically engineered mice to study the AgRP hunger neurons, finding that fasting activates these cells, while food cues inhibit their activity. The team discovered that the aversive feeling caused by hunger enhances learning, making dieting difficult due to this persistent sensation.
A diet rich in isoflavone may provide protection against multiple sclerosis-like symptoms when combined with specific gut bacteria that can break down the compound. The study found that mice fed an isoflavone diet had a microbiome similar to healthy individuals, while those without it lacked beneficial bacteria.
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Researchers at Kobe University have identified a causal gene, Necdin (NDN), associated with autism spectrum disorder and other developmental disorders. The study reveals that the NDN gene regulates synapse development during critical developmental stages.
Scientists from the Netherlands Institute for Neuroscience found that mice have a region called 'focea' with improved visual sensitivity, similar to the fovea in human retinas. This discovery suggests that mice may be better models for studying human vision than previously thought.
Researchers found that playing broadband sounds during the onset of congenital hearing loss preserved auditory processing of time-related sound features. The intervention also prevented hair cells from dying and maintained sound processing function in brainstems, cochleas, and midbrains.
A team of researchers from Japan and Germany created a mouse model that mimics the human pathology of restrictive cardiomyopathy, allowing for easier study. The model shows changes in protein quality control and autophagy, leading to fibrosis and heart muscle stiffening.
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Researchers discovered that a Western diet high in fat and cholesterol can lead to obesity, diabetes, and Non-alcoholic steatohepatitis (NASH), which progresses to liver cancer, kidney disease, and cardiovascular disease. Switching to a normal chow diet improves NASH and liver fibrosis, prevents cancer progression and mortality.
Researchers have discovered a novel consortium of bacteria that can prevent and treat chronic immune-mediated colitis in humanized mouse models. The treatment targets the source of inflammatory bowel disease, restoring normal gut function and reducing symptoms.
The La Jolla Institute for Immunology has partnered with Synbal, Inc. to develop multi-gene, humanized mouse models for COVID-19 research. These new models are expected to provide a better understanding of SARS-CoV-2 infection and disease severity, enabling the development of more effective vaccines and therapies.
Scientists have discovered a novel deafness gene, TMEM43, linked to auditory neuropathy spectrum disorder (ANSD), a rare form of hearing loss that affects speech comprehension. The treatment involves cochlear implants, which have successfully restored speech discrimination in patients, offering new hope for those affected.
Researchers developed a unique pre-clinical model of long-term HIV infection using subset of human CD4 cells, excluding those prone to attacking mouse tissue. The model showed that memory CD4 cells can be infected and killed by HIV or protected by anti-HIV drugs, paving the way for T-cell based therapies
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.