Articles tagged with Microglia
Researchers explore the role of efferocytosis in reducing inflammation and containing injury spread after an ischemic stroke. Efferocytosis may offer a promising therapeutic strategy to promote neural regeneration and minimize brain damage.
Researchers have unveiled a critical mechanism linking cellular stress in the brain to Alzheimer's disease progression, highlighting microglia as central players in both protective and harmful responses. The study reveals that blocking a specific stress pathway reverses symptoms of Alzheimer's disease in preclinical models.
Ocular immune-related diseases, including uveitis, diabetic retinopathy, age-related macular degeneration, and Graves' ophthalmopathy, are caused by abnormal immune inflammatory responses. The review highlights the role of microglia and other macrophages in these conditions, providing new target cells for prevention and treatment.
Researchers found that microglia clear amyloid-β plaques from the brain before plaque formation and may cause more plaques when homeostatic. In contrast, activated microglia help compact plaques in neurons, offering a protective role.
Researchers uncover the significance of neuroinflammation in Niemann-Pick type C disease, a rare form of childhood dementia. They identify translocator protein (TSPO) as a potential biomarker for disease monitoring and response to therapy.
Researchers have developed a network-based approach to understand how immune cells called microglia transform and drive harmful processes like neuroinflammation in Alzheimer's disease. The study identified three unique subtypes of harmful microglia that promote disease progression, with genetic signatures driving their behaviors.
Researchers at Texas A&M University College of Medicine have developed a nasal spray treatment using stem cell-derived vesicles that reduces inflammation and plaque buildup in the brain, delaying Alzheimer's disease progression. The treatment targets microglia cells, which become harmful over time, leading to progressive neuron loss.
Chronic neuroinflammation, driven by activated microglia and astrocytes, is a hallmark of neurodegenerative diseases. Targeted therapies that modulate microglial and astrocytic activity show promise in mitigating neuroinflammation.
Researchers at Gladstone Institutes created a new mouse model to study Alzheimer's disease, transplanting human neurons into mouse brains. The study found that immune cells called microglia cause harmful inflammation and clumps of misfolded proteins when interacting with the APOE4 protein.
Researchers at HKUST have discovered a neuroprotective mechanism involving microglia that prevents acute axonal degeneration after spinal cord injury. Microglia establish direct contact with myelinated axons, exhibiting a protective wrapping behavior that delays degeneration.
Researchers found that low extracellular sodium concentrations decrease specific mRNA expression and nitric oxide production in microglia, potentially contributing to hyponatremia-induced neuronal dysfunctions. Microglial activation can lead to inflammation and regulate neurotransmission.
A Trinity scientist has won an ERC Starting Grant to investigate the role of microglia in brain disorders. The project aims to create a detailed map of how these immune cells change during brain damage, disease, or repair, with the goal of developing methods to control and rejuvenate neuropathology.
Researchers investigate how hypernatremia affects microglial responses and evaluate potential therapies. Microglia's response to hyperosmotic stress is found to be associated with NFAT5 expression and NO production.
A University of Oklahoma researcher is investigating how prenatal inflammation increases the risk of neurodevelopmental disorders like ADHD and autism. She hopes to find a way to promote fetal resilience to inflammation using antioxidants like PQQ.
Microglia establish contact with neurons through tunnelling nanotubes to clear toxic protein aggregates, reducing oxidative stress and restoring vital functions. Healthy mitochondria are also transferred from microglia to affected neurons, preserving energy production and neuronal survival.
Researchers found that a cancer drug can restore phagocytosis, a process crucial for brain health, in individuals with Rett syndrome by targeting microglia. The study highlights the potential therapeutic target of microglia in neurological conditions and may lead to new treatments.
A breakthrough near-infrared photobiomodulation technique has shown potential in suppressing neuroinflammation and promoting microglia cell proliferation. The study's findings suggest that LEDs with broadband NIR emission could offer a cost-effective, side-effect-free treatment option for millions suffering from neurodegenerative disea...
A new University of Cincinnati study reveals that a signaling pathway in the brain helps maintain health and prevent inflammation and cognitive deficits. Microglia cells produce their own TGF-β ligand to regulate local states of inflammation.
Researchers at Harvard University have identified a specific cell type in the mouse embryonic brain that responds to an immune response in the mother, altering gene regulation and persisting in juvenile mice. This study provides new insights into how maternal immune responses might influence brain development in embryos, potentially sh...
New research reveals exercise reverts aged microglia gene expression patterns to those of young microglia, supporting the formation of new neurons in the hippocampus. Exercise also reduces T cell accumulation in the brain, a common feature of aging.
Researchers at the University of Seville discovered Galectin-3's crucial role in brain tumour progression, finding its inhibition significantly reduces glioblastoma size and brain metastases. Inhibition promotes pro-inflammatory markers and reverses immunosuppressive biomarkers, leading to improved outcomes.
A new study from Brigham and Women's Hospital suggests that PET brain scans can detect hidden inflammation in MS patients who are being treated with highly-effective treatments. The findings indicate that smoldering inflammation may linger in patients, driving disease progression and symptoms.
A study using a xenotransplantation model has revealed that human microglia respond to amyloid-β plaques with a complex immune response, influencing the disease course. The research highlights the importance of considering genetic factors in microglia-targeted therapies for Alzheimer's disease.
Researchers at University of Pittsburgh are developing a platform to genetically modify glia cells using bioengineering modified RNAs. The goal is to increase or decrease disease-relevant genes in astrocytes or microglia to potentially treat Alzheimer's disease and other neurodegenerative disorders.
Researchers at Mount Sinai School of Medicine have identified macrophages as crucial in clearing lipid-rich waste from the brain. By studying genes controlling these immune cells, they discovered that two specific genes BHLHE40 and BHLHE41 regulate their activity.
A Mayo Clinic study found that microglia shield neurons from the aftereffects of anesthesia, enhancing and boosting neuronal activity to awaken the brain. This discovery could lead to new treatments for post-anesthesia delirium and hyperactivity.
Researchers have identified a genetic variant in SIRPβ1 gene that affects the immune system's response to beta-amyloid deposits, leading to altered Alzheimer's disease progression. The mutation has been shown to increase cognitive decline in early stages but slow it down in advanced stages.
Researchers develop nanovector nanogels that selectively target glial cells involved in spinal cord injury inflammation, reducing damage and improving recovery. The treatment demonstrates potential for modulating glial cells in neurodegenerative diseases like Alzheimer's.
Researchers found that low-dose X-ray irradiation reduced lesion size and reversed motor deficits in TBI and ischemic stroke mice, demonstrating its potential as a therapeutic strategy. The treatment also accelerated substantial motor function recovery and promoted brain rewiring after stroke.
A novel cell-penetrating peptide, Tat-SIRT5-CTM, has been shown to reduce brain infarct area and neuronal loss in a mouse model of ischemic stroke. The peptide inhibits microglia-induced neuroinflammation by promoting ANXA1 nuclear translocation.
Researchers at the University of Rochester Medical Center find that microglia can trigger cognitive deficits after radiation exposure, potentially targeting them for therapy development. Mice studies showed that blocking a specific pathway in microglia prevented cognitive decline, offering hope for improving patients' quality of life.
Researchers discovered that microglia regulate neuronal activity in a brain region-specific manner, playing a key role in how anesthesia works. Microglia depletion delayed induction and led to early emergence of anesthesia.
Researchers developed novel nanoparticles that deliver RNA to microglia immune cells, reducing inflammation linked to Alzheimer's disease. The study showed a 42% reduction of PU-1 expression and multiple inflammatory markers in human cell cultures and mice models.
Researchers found that a rare genetic mutation in the APOE gene, known as the Christchurch mutation, may prevent Alzheimer's dementia by severing the link between amyloid and tau accumulation. This discovery offers new hope for preventing the disease.
Researchers found an inverse relationship between axon loss and demyelination, suggesting that 'bad' myelin can be more damaging than its absence. This study identifies potential therapeutic targets for diseases associated with myelin defects and inflammation in the nervous system.
A study by Brigham investigators found that genetic changes in microglia contribute to neuroinflammation, a key factor in Alzheimer's disease progression. Lower levels of INPP5D gene led to increased inflammation and risk for AD.
A new study reveals that a genetic mutation in microglia can elevate Alzheimer's risk by reducing brain circuit connections, promoting inflammation, and impairing debris clearance. The mutation affects the TREM2 protein, leading to increased expression of inflammatory genes and impaired response to neuron injury.
Scientists have found that microglia play a crucial role in regulating the number of cells that become neurons in the brain, enhancing our understanding of brain development and disorders. The discovery also reveals a unique pathway through which microglia interact with other brain cells, involving cholesterol transfer.
A new study suggests that hormonal birth control used by adolescents may influence the development of their brain, leading to altered risk assessment. The researchers found increased myelination and decreased immune cells in the brains of treated rats, while also exhibiting signs of impulsivity in behavior tests.
Researchers at Ohio State University will investigate the role of microglia cells in chronic inflammation and neuronal dysfunction after TBI, with a focus on preventing long-term consequences. The $7.7 million award aims to develop innovative healthcare solutions for traumatic brain injury survivors.
Researchers found changes in microglial cells, a specialized subset of immune cells, that may worsen schizophrenia risk in adolescents. The study, published in Nature Communications, suggests that THC exposure during adolescence can lead to long-lasting negative effects on brain development and function.
Researchers have discovered axonal dysregulation in the prenatal brain as a mediator of genetic risk for schizophrenia. The study used induced pluripotent stem cells and three-dimensional brain organoids to identify key genes involved, including CYFIP1, which is highly expressed in microglia.
Researchers at Kyushu University have successfully converted brain immune cells into neurons, which restored brain function after a stroke-like injury in mice. The findings suggest that replenishing neurons from immune cells could be a promising avenue for treating stroke in humans.
Researchers have discovered new insights into microglia-astrocyte communication and its impact on intracerebral hemorrhage, as well as the testicular toxicity of triptolide. Additionally, a study on epicardial cells has identified key gene markers associated with cardiac regenerative therapy strategies.
A recent study published in Nature Medicine suggests that complement proteins and microglia can be activated early in the development of Huntington's Disease, leading to synapse loss and cognitive decline. By blocking these proteins, researchers were able to prevent or slow cognitive defects and motor symptoms in animal models.
Scientists at Temple University's Alzheimer's Center have identified a promising new therapeutic target for Alzheimer's disease: the protein ABCA7. The study found that cholesterol depletion and inflammation suppress ABCA7 levels in human brain cells, potentially contributing to disease onset.
Researchers identify somatostatin-positive interneurons as crucial in maintaining cognitive function, and their dysfunction leads to impaired memory and learning. The study uses a toxin to ablate these cells, resulting in mice exhibiting cognitive deficits similar to those seen in aging humans.
Researchers analyzed over 2 million cells from 400 postmortem brain samples to identify cellular pathways that could become new drug targets for Alzheimer's treatments. They found impairments in mitochondrial function, synaptic signaling, and protein complexes, as well as disrupted lipid metabolism.
A recent study by Ohio State University researchers found that saturated fats can interfere with the creation of new memories in aged brains. However, omega-3 fatty acids, particularly DHA, may help protect brain cells from fat-related inflammation. The study used cell cultures and brain tissue from aging mice to explore the effects of...
An international team has decoded the TSPO protein to visualize neuroinflammation, revealing its relationship with microglial cells. The study's findings pave the way for optimizing observation of neuroinflammatory processes and re-reading previous studies.
Scientists have identified thousands of non-coding genetic variants linked to Alzheimer's disease, focusing on their impact on microglial gene expression and function. The study found that turning off specific regions can affect multiple genes, highlighting the complex mechanisms underlying AD.
Microglial cells age differently in male and female mice, with female microglia displaying a 'middle-aged' phenotype and male microglia switching suddenly to an aged phenotype. The researchers identified key genes and mechanisms contributing to this aging process, including the role of aged-like microglia in cognitive decline.
The collaboration has garnered $5.68 million of grant support, with a five-year $2.13 million National Institutes of Health R01 grant and a five-year $2.89 million NIH R01 grant. Researchers are using computational biology to model a key Alzheimer's protein called TREM2 and its interactions with small chemical molecules.
Researchers at St. Jude Children's Research Hospital discovered a subset of immune cells that slows Alzheimer's disease progression by interacting with microglia. The cells, called CD8+ T cells, use a molecular handshake to signal to the microglia to stop causing uncontrolled inflammation, which in turn slows plaque growth and symptoms.
Researchers found that ferroptosis, a form of cell death caused by iron buildup, destroys microglia cells in the brain's immune response, contributing to cognitive decline. The study's findings may lead to the development of compounds targeting microglial degeneration, offering new hope for Alzheimer's and vascular dementia treatments.
Researchers have identified a new cell type, ARG1+ microglia, involved in brain development and function during early postnatal stages. This discovery sheds light on the role of microglia in neural systems and their potential link to neurodevelopmental and neurodegenerative diseases such as Alzheimer's.
A new molecule called A11 has been found to reduce inflammation and improve memory in models of Alzheimer's disease. By targeting the genetic transcription factor PU.1, A11 suppresses inflammatory gene expression in microglia immune cells, leading to reduced neurodegeneration and improved cognition.
Researchers have successfully transplanted human microglia cells into mouse retina, creating a model for studying treatments for diabetic retinopathy, glaucoma, and age-related macular degeneration. The study demonstrates the potential of microglial replacement therapy to treat retinal and central nervous system diseases.
Researchers find immunotherapy treatment anti-CTLA-4 leads to greater survival in mice with glioblastoma and discover new way cells kill cancer by triggering microglia, specialized immune cells in the brain. This breakthrough could lead to more effective treatments for human brain cancer.
A study found that border-associated macrophages play a crucial role in neuroinflammation and neurodegeneration in Parkinson's disease. Deleting MHCII from these cells reduced neuroinflammation, suggesting they are essential for presenting alpha-synuclein antigens to T cells.