Articles tagged with Microglia
Comprehensive exploration of living organisms, biological systems, and life processes across all scales from molecules to ecosystems. Encompasses cutting-edge research in biology, genetics, molecular biology, ecology, biochemistry, microbiology, botany, zoology, evolutionary biology, genomics, and biotechnology. Investigates cellular mechanisms, organism development, genetic inheritance, biodiversity conservation, metabolic processes, protein synthesis, DNA sequencing, CRISPR gene editing, stem cell research, and the fundamental principles governing all forms of life on Earth.
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Fundamental study of the non-living natural world, matter, energy, and physical phenomena governing the universe. Encompasses physics, chemistry, earth sciences, atmospheric sciences, oceanography, materials science, and the investigation of physical laws, chemical reactions, geological processes, climate systems, and planetary dynamics. Explores everything from subatomic particles and quantum mechanics to planetary systems and cosmic phenomena, including energy transformations, molecular interactions, elemental properties, weather patterns, tectonic activity, and the fundamental forces and principles underlying the physical nature of reality.
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Study of the practice, culture, infrastructure, and social dimensions of science itself. Addresses how science is conducted, organized, communicated, and integrated into society. Encompasses research funding mechanisms, scientific publishing systems, peer review processes, academic ethics, science policy, research institutions, scientific collaboration networks, science education, career development, research programs, scientific methods, science communication, and the sociology of scientific discovery. Examines the human, institutional, and cultural aspects of scientific enterprise, knowledge production, and the translation of research into societal benefit.
Comprehensive study of the universe beyond Earth, encompassing celestial objects, cosmic phenomena, and space exploration. Includes astronomy, astrophysics, planetary science, cosmology, space physics, astrobiology, and space technology. Investigates stars, galaxies, planets, moons, asteroids, comets, black holes, nebulae, exoplanets, dark matter, dark energy, cosmic microwave background, stellar evolution, planetary formation, space weather, solar system dynamics, the search for extraterrestrial life, and humanity's efforts to explore, understand, and unlock the mysteries of the cosmos through observation, theory, and space missions.
Comprehensive examination of tools, techniques, methodologies, and approaches used across scientific disciplines to conduct research, collect data, and analyze results. Encompasses experimental procedures, analytical methods, measurement techniques, instrumentation, imaging technologies, spectroscopic methods, laboratory protocols, observational studies, statistical analysis, computational methods, data visualization, quality control, and methodological innovations. Addresses the practical techniques and theoretical frameworks enabling scientists to investigate phenomena, test hypotheses, gather evidence, ensure reproducibility, and generate reliable knowledge through systematic, rigorous investigation across all areas of scientific inquiry.
Study of abstract structures, patterns, quantities, relationships, and logical reasoning through pure and applied mathematical disciplines. Encompasses algebra, calculus, geometry, topology, number theory, analysis, discrete mathematics, mathematical logic, set theory, probability, statistics, and computational mathematics. Investigates mathematical structures, theorems, proofs, algorithms, functions, equations, and the rigorous logical frameworks underlying quantitative reasoning. Provides the foundational language and tools for all scientific fields, enabling precise description of natural phenomena, modeling of complex systems, and the development of technologies across physics, engineering, computer science, economics, and all quantitative sciences.
Scientists have identified a specific antibody that binds to brain immune cells and triggers processes that enhance microglia activity. This stimulates the immune cells to detect and degrade abnormal protein deposits, known as plaques, more effectively, potentially providing better protection against Alzheimer's disease.
Researchers found a polymorphism associated with protective effects against major depressive disorder in women. Microglial cells' immune receptors may play a role in neuropsychiatric disorders.
Researchers found that rejuvenating immune cells, specifically microglia, significantly improved brain repair and learning abilities in animal models. This discovery challenges the long-held assumption that microglia drive inflammation after brain injuries.
Visceral fat generates high levels of interleukin-1 beta, over-activating microglia and promoting chronic inflammation. This leads to impaired cognitive function, including difficulties with navigation and learning and memory.
A study published in Nature Communications reveals that microglia can both protect and damage the blood-brain barrier, depending on the level of systemic inflammation. The researchers used fluorescent labeling and two-photon imaging to study the interactions between microglia and the blood-brain barrier.
A preclinical study suggests that targeting overactive immune cells in the brain can limit brain cell loss and reverse cognitive and motor difficulties caused by traumatic brain injury (TBI). Mice treated with an experimental drug recovered markedly better than control mice, showing less tissue loss and improved motor and cognitive per...
New preclinical research suggests that targeting overactive immune cells can improve traumatic brain injury recovery and modulate chronic neurotoxic effects. The study found that a therapeutic strategy to inhibit microglia cells after TBI led to better motor and cognitive performance in mice.
Researchers at RMIT University found that microglia cells can be activated to boost memory performance in rats by up to 50%, reversing damage caused by neuroinflammation. This discovery could lead to the development of new treatments for cognitive decline and dementia.
A recent study has shown that microglia regulate forgetting in the adult brain by weakening and eliminating synapses connecting engram neurons. Inhibiting microglial activity or depleting them prevents forgetting, while intact microglia facilitate the dissociation of engram cells, leading to memory erasure.
Researchers found that microglia, immune cells in the brain and central nervous system, encase macrophages, preventing them from dispersing into areas they shouldn't be. This discovery may lead to new treatments for conditions like multiple sclerosis and Alzheimer's disease.
Researchers at UMass Chan Medical School have developed a gene therapy approach that protects synaptic connections in the brain from damage in multiple sclerosis models. The study suggests that therapies targeting specific circuits of the brain could be effective in preserving vision and preventing neurodegenerative symptoms.
Researchers found that radiation triggers an immune response that severs connections between nerve cells, leading to damage and cognitive problems. The study suggests two potential approaches to prevent this damage: blocking a receptor responsible for synapse removal or tamping down the brain's immune response.
A study by University of Alberta chemists identifies CD33 protein as a factor that may decrease the likelihood of Alzheimer's disease. The most common type of CD33 protein plays a crucial role in modulating microglia function, which can protect against neurodegenerative plaques.
A team of international researchers has identified a potential treatment for reducing brain injury in premature babies by targeting hyperactive microglia with a drug that activates the Wnt signalling pathway. This approach may help protect white matter and prevent long-term memory problems associated with preterm birth.
Researchers found a correlation between dysfunctional microglia and obsessive-compulsive disorder (OCD) behaviors in mice. Female sex hormones exacerbated symptoms, indicating a potential genetic link to anxiety disorders.
Researchers have made significant breakthroughs in understanding the role of microglia in neuroinflammation, a hallmark of degenerative brain diseases such as Alzheimer's Disease. Studies show that changes in microglial cells can trigger hyperexcitability in the brain, leading to decreased sociability and motivation.
New research reveals that immune cells called microglia are active during sleep, rewiring brain connections and repairing damage. Microglia's interaction with neurotransmitters like norepinephrine regulates their activity, suggesting a link between sleep and brain health.
Research in animals shows that chronic stress during pregnancy triggers an immune response in the brain, leading to potential changes in brain functions. The study found that stressed rats showed evidence of neuroinflammation and increased activity levels of microglia, suggesting a link between gestational stress and postpartum depress...
A recent study has identified a key regulator of microglia function during inflammation, which could become a significant component in treating neurodegenerative diseases. TET2 protein modulates the immune response generated by microglia cells in the brain under inflammatory conditions.
A new study found that brain immune cells called microglia drive brain damage in Alzheimer's patients. Eliminating these cells reduces tau-linked brain damage, suggesting a potential therapeutic target.
A study published in the journal Aging Cell found that a lifelong dietary regimen of choline can improve spatial memory and reduce AD-like symptoms in female mice. Choline supplementation also reduces microglia activation, offering protection from brain inflammation and neuronal death.
A new study reveals that APOE4, the strongest genetic risk factor for Alzheimer's disease, impairs the function of human brain immune cells, microglia. This impairment increases inflammation and reduces their ability to remove toxic amyloid from the brain.
Researchers discovered LH dipeptide as a potent anti-inflammatory agent that inhibits the secretion of inflammatory cytokines from microglia, reducing brain inflammation and depression symptoms. Consuming foods rich in LH dipeptide may be a safe method for maintaining good mental health.
A recent Yale study found that high-fat diets stimulate hypothalamic inflammation, leading to changes in microglial cells and regulating energy homeostasis. The research suggests a neurological mechanism controlling food intake, with potential implications for obesity and diseases like Alzheimer's.
Researchers discovered that higher levels of TREM2 protein in cerebrospinal fluid are associated with improved prognosis and reduced cognitive decline in Alzheimer's patients. The study suggests that TREM2 may play a key role in regulating the brain's protective immune response, offering new therapeutic strategies.
Researchers discovered that removing brain immune cells called microglia prevents beta-amyloid plaque formation in rodent models of Alzheimer's. This finding suggests a crucial role for microglia in the disease's development and progression.
Researchers at UCI have developed a mouse model that allows for the study of human brain immune cells in unprecedented detail. The 'chimeric' mouse contains human microglia, enabling the investigation of Alzheimer's mechanisms and potential treatments.
Researchers at Massachusetts General Hospital discovered a key gene interaction that fuels neuroinflammation, leading to cognitive decline and Alzheimer's disease. CD33 and TREM2 genes regulate microglia activity, with CD33 acting as the 'on' switch for inflammation.
The study reveals Galectin-3 plays a key role in regulating immune response associated with Amyloid beta peptide. Researchers have identified genetic mutations linked to increased risk of Alzheimer's, and a potential therapeutic target for blocking galectin-3.
A study has identified a key connection between two damaging proteins in Alzheimer's disease: amyloid beta and tau. Immune cells called microglia may be the missing link between these proteins, which can cause brain tissue damage.
Researchers have developed a microglia-selective fluorogenic probe that triggers fluorescence through gene expression, enabling selective labeling and imaging of microglia cells in live brain tissue. This probe has the potential to detect developing neural diseases such as Alzheimer's disease and stroke.
Researchers found that visual stimulation can prevent neuron degeneration and enhance synaptic function in Alzheimer's disease models. The treatment also improved spatial memory performance in older mice without a predisposition for the disease.
A new study uncovers the presence of 'hidden' microglia in the brain, which show a resemblance to microglia associated with Alzheimer's disease. The researchers hope to find strategies for controlling these immune cells to develop future treatments for neurodegenerative diseases.
Researchers developed a chemical probe that enables live-imaging of microglia in the brain, crucial for understanding brain development and disease. The probe, CDr20, labels microglia in both human- and primate-derived cells, allowing for clinical-relevant studies.
Researchers studied how microglia cells in the brain respond to toxic proteins associated with Alzheimer's disease. The study found that age, sex, and genetics affect microglial response, suggesting that modulating this response could lead to new treatments.
Researchers at Mass Eye and Ear have identified microglia as gatekeepers that orchestrate inflammatory responses in the retina during autoimmune uveitis. By depleting microglia, disease was completely blocked, suggesting a novel therapeutic target for this devastating eye disease.
A new study by University of Notre Dame scientists reveals microglia can cross from the central nervous system (CNS) into the peripheral nervous system (PNS) in response to injury. This finding has broad implications for nervous system diseases and opens up new questions about the function and capabilities of these cells.
A Stanford University School of Medicine study found that blocking a specific protein's activity improved cognitive behavior in aging mice. The researchers identified a gene called CD22, which is involved in microglial phagocytosis and is upregulated with age.
Scientists discovered that microglia, a type of nervous system cell suspected to cause retinal damage, surprisingly had no damaging role during prion disease in mice. Microglia might delay disease progression, providing new insights into inherited photoreceptor degeneration diseases.
Researchers created a high-resolution map of the brain's immune system, showing that all microglia have the same core signature but adapt differently depending on their function. This discovery is significant for understanding brain diseases like multiple sclerosis and Alzheimer's.
A study published in Nature Neuroscience found that individuals with schizophrenia exhibit excessive synaptic pruning, a process normally occurring during adolescence. This abnormality contributes to the development of schizophrenia symptoms.
Researchers at the National Eye Institute discovered that TGF-beta signaling governs immune cell function in the eye, leading to activated microglia and retina damage. Disrupting this signal may represent a potential therapeutic target for treating AMD.
A study published in Nature Neuroscience reveals that defective immune cells in the brain play a key role in Alzheimer's disease. Activating a specific gene, TREM2, can help prevent toxic deposits, but over-activation may have negative consequences.
Researchers at Arizona State University discover that choline supplementation may help fight Alzheimer's disease in mice and their offspring. The study reveals that high choline intake during gestation and lactation improves spatial memory in subsequent generations, suggesting a transgenerational effect.
Research found that activation of microglia in the spinal cord is responsible for increased pain sensitivity in response to stress. Eliminating microglia from the spinal cord prevented these effects, highlighting their role in transmitting pain to the brain.
Researchers at Johns Hopkins Medicine found that the molecular underpinnings of necrotizing enterocolitis (NEC) lead to brain injury. They identified TLR4 as the cause and found that HMGB1 is generated in response to TLR4, leading to microglial activation and brain injury.
Researchers have identified nine distinct groups of microglia, including some that appear only in embryonic or newborn stages, and others that are involved in myelination. These findings may help uncover new roles for microglia in disease and development, and could lead to the development of therapies targeting specific subpopulations.
Researchers at The Ohio State University found that eliminating microglia can reverse some aspects of stress sensitization, but not increased anxiety. Microglia hold unique signatures of chronic stress and play a critical role in the recurrence of anxiety after chronic stress.
Researchers from the Luxembourg Institute of Health uncover distinct microglial signatures in response to acute inflammation, highlighting potential benefits for resolving inflammation. Their single-cell transcriptomic study provides new resources for understanding brain disorders and developing novel therapeutic strategies.
A study in mice found that eliminating microglia cells eliminated inflammation following traumatic brain injury, offering a potential target for treatment. The research aims to understand cellular-level changes associated with sports-related concussion and other brain injuries.
Targeting immune checkpoints in microglia may reduce neuroinflammation in neurodegenerative diseases. Dysregulation of these checkpoints is linked to diseases such as Alzheimer's, Parkinson's, and ALS.
Researchers at Boston Children's Hospital have discovered a 'don't eat me' signal that prevents microglia from pruning useful connections. This 'yin/yang' system helps fine-tune brain circuits, ensuring normal brain development and potentially treating neurodegenerative diseases.
Researchers at MassGeneral Hospital for Children found that microglia play a crucial role in shaping behavior during adolescence, with different effects in males and females. The study suggests that this process could improve understanding of normal behavioral changes and neuropsychiatric disorders that emerge during adolescence.
A new study from the University of Illinois found that dietary fiber can reduce brain inflammation in old mice, leading to improved memory and reduced cognitive decline. The researchers discovered that high-fiber diets elevated butyrate levels in the blood, which had anti-inflammatory properties on microglia.
Research reveals obesity activates microglia, consuming healthy synapses and leading to dendritic spine loss. Microglial activity is causally linked to obesity-induced cognitive decline, suggesting a potential therapeutic target for this condition.
Researchers found that ACE inhibitors can block the activation of brain cells called microglia, which contribute to memory loss and cognitive impairments in SLE patients. The study suggests that these drugs may be used to preserve the memory of lupus patients.
Researchers at Max Delbrück Center for Molecular Medicine found significant differences in male and female mice microglia structure and function. Male microglia are more active and respond differently to injury, but may also be less protected against environmental insults.
Chronic inflammation caused by failed sensor mechanism can lead to brain cells' loss in old age. The study suggests that CB1 receptors on neurons control microglial cell activity.
Researchers discovered that brain microglia clearance activity in different regions goes hand in hand with natural neuronal degeneration. Microglia can mistakenly attack healthy neurons if their 'eating' behavior is turned on inappropriately, leading to cellular changes associated with neurodegenerative diseases.
Researchers identified a molecular key, P2X4 receptor, that delays Multiple Sclerosis (MS) progression by reducing chronic inflammation and promoting repair responses in the nervous tissue. The study found that activating this receptor improves symptoms during the disease's chronic phase.