Articles tagged with Microglia
A recent study by McGill University Health Centre researchers found that microglia can reduce the adverse changes to neural circuitry caused by chronic cocaine use. Microglia may be enticed to keep going by stimulating their production of TNF, which suppresses synaptic changes caused by cocaine.
Salk scientists discovered that specific immune receptors in the brain play a crucial role in clearing both healthy and dying neurons. In their absence, new neurons increased dramatically in certain regions, suggesting that these receptors may also target living but dysfunctional cells.
A new study reveals that a targeted immune pathway may be the key to preserving cognitive function in Alzheimer's disease. By blocking this pathway, researchers were able to reduce synapse loss in mouse models of the disease, offering hope for a potential therapeutic target to halt its progression.
A new study reveals that immune cells called microglia play a crucial role in rewiring brain connections, a process essential for neuroplasticity and learning. By 'pruning' unwanted connections, microglia enable the formation of new pathways between neurons.
A new biomarker of brain inflammation in early-stage Alzheimer's disease has been identified, indicating that microglia-mediated inflammation may demarcate the transition from preclinical to full dementia. The TREM2 protein fragment in cerebrospinal fluid levels closely mirror microglia activity during the course of the disease.
Researchers have identified a new biomarker associated with the activation of an innate immune response to neural damage during early stages of Alzheimer's disease. The concentration of a specific segment of the protein TREM2 in cerebrospinal fluid is significantly elevated in early stages of the disease.
Researchers found that flushing away inflammatory cells contributed to restored memory function in test mice with Alzheimer's disease. The study suggests targeting these cells with specific drugs may be a promising new approach.
Researchers identify microglia cells as primary cause of cognitive problems in MS patients, disrupting communication between nerve cells. The findings suggest that the disease's impact on cognition is more complex than previously thought, with potential new targets for treatment.
The study found that microglia, the brain's immune system, rapidly repair damage to the blood-brain barrier after breaches. This process could be impaired by certain cardiovascular drugs intended to prevent stroke-related damage.
A University of Southampton-led study found that blocking a receptor in the brain responsible for regulating immune cells can prevent cognitive decline and memory loss associated with Alzheimer's disease. The researchers discovered that reducing brain inflammation could halt disease progression.
A new study suggests that the brain's immune system can be harnessed to clear amyloid plaques, a hallmark of Alzheimer's disease. Microglia, native brain cells, play a key role in this process, and manipulating their activation may accelerate plaque removal.
Researchers from Hebrew University of Jerusalem suggest that microglia cells may be a key to causing depression, leading to potential new treatments. The study proposes a personalized medical approach using drugs that restore normal microglia function to diagnose and treat depression.
A team of researchers at Charité - Universitätsmedizin Berlin found that peripheral macrophages can be repurposed to clean up beta-amyloid deposits in the brain. However, even with stimulation, these cells were ineffective and require further investigation into a missing stimulus.
A study from the Gladstone Institutes reveals that a single drop of blood in the brain can trigger an autoimmune response akin to multiple sclerosis. Fibrinogen, a blood-clotting factor, activates microglia and recruits peripheral immune cells, causing myelin damage and inflammation.
Microglia facilitate the spread of tau fibrils between neurons by releasing exosomes, which could lead to a novel therapeutic target for Alzheimer's disease. Pharmacologic depletion and inhibition of exosome production suppress tau spread, restoring neural excitation.
Researchers found iron-laden microglia in specific brain regions of Alzheimer's patients, which could aid in earlier diagnosis and monitoring using advanced MRI techniques. The study suggests a new suspect for the disease, contradicting the long-held hypothesis that amyloid plaques are the primary cause.
Researchers found that microglia infiltrate the retina and create a cup-like structure over photoreceptors, accelerating their death. Inhibiting phagocytosis or targeting microglial activation may help preserve vision in retinitis pigmentosa.
Researchers found that male and female mice process pain using different cells, with female mice relying on T cells to sound the pain alarm. This discovery has far-reaching implications for developing targeted pain medications and highlights the need for more inclusive preclinical research.
A novel PET technique tracks microglial activation in response to endotoxin, shedding light on neuroinflammatory diseases like Alzheimer's and depression. The study's findings could lead to new drug treatments by targeting immune dysfunction.
Researchers have identified a key role for microglia in the development of chronic pain, including hyperalgesia and allodynia. Microglia-to-neuron signaling is crucial for these effects, which could lead to new treatments for chronic pain.
A new study finds that carbon monoxide can help accelerate the natural process of clearing heme, a toxic component of red blood cells, and reduce neuronal injury in mice with subarachnoid hemorrhage. The study suggests that low amounts of CO may be used to treat patients with ruptured cerebral aneurysms.
A team of neuroscientists found that misfolded a-synuclein can activate microglia, leading to chronic inflammation. They also identified specific receptors on microglial cells that respond to the protein and tested drugs to reduce inflammation.
Researchers at UCSF discovered that immune cells in brain respond to fat in diet by causing mice to consume more food. The study found that a population explosion of microglia, a type of immune cell, in the hypothalamus region drives increased food intake.
Researchers at Stanford University School of Medicine found that blocking a single molecule on microglia restored their function, reversing memory loss and other Alzheimer's-like features in mice. The study suggests that microglia play a crucial role in clearing A-beta protein clusters, which contribute to the disease's progression.
Recent studies have shown that microglia-conditioned culture medium supports OPCs' survival and enhances their differentiation. The role of microglia in remyelination is complex and varies depending on the timing of disease progression. Microglia/macrophage activation can lead to poor remyelination in MS plaques lacking microglia.
A common genetic defect affects neurodegenerative diseases like Alzheimer's and Parkinson's by impairing microglial waste removal. This leads to accumulation of toxic protein deposits, triggering inflammatory reactions that promote further nerve-cell loss.
Researchers found that immune cells in the central nervous system of elderly mice fail to activate an important signaling pathway, lowering chances for repair after spinal cord injury. In contrast, young adult mice showed a functional repair response.
Ginsenoside Rb1 attenuates damage to cerebral cortex neurons by downregulating nitric oxide, superoxide, and tumor necrosis factor-α expression in hypoxia-activated microglia. The study suggests that ginsenoside Rb1 is a promising candidate for clinical use in preventing neuronal degeneration following cerebral ischemia.
A new study by Nationwide Children's Hospital researchers has identified a potential culprit in the death of motor neurons in Lou Gehrig's disease. Inhibiting nuclear factor-kappa B (NF-ƘB) in microglia slowed disease progression by 47 percent, suggesting a new target for ALS treatment.
Researchers discovered the mechanisms behind long-term depression, a cognitive impairment contributor to Alzheimer's disease. Chronic inflammation and hypoxia activate microglia, weakening neural connections.
Regular exercise and surgical removal of belly fat can improve cognition in obese, diabetic mice by reducing inflammation in the brain's hippocampus. Obesity and diabetes increase the risk of mild cognitive impairment and Alzheimer's disease.
Researchers at European Molecular Biology Laboratory identify microglia cells as major players in brain wiring and behavior. Mice with fewer microglia display weaker connections between neurons and repetitive behaviors associated with autism spectrum disorders.
Researchers at Hebrew University find that chronic stress activates microglia cells, leading to depressive-like behavior and reduced neurogenesis. Blocking or stimulating microglia cells with specific drugs can reverse these effects, offering new avenues for antidepressant treatment.
A new study suggests that a head injury can lead to depressive complications years later due to an overactive immune response and inflammation. The research found that brain cells went on 'high alert' after the injury, affecting behavior and leading to symptoms that were linked to inflammation.
A team of researchers has discovered a mechanism that boosts the immune system and reduces brain tumor growth, paving the way for new treatment options. The study identified a commercially available drug, amphotericin B, as a potential novel treatment for patients with glioblastoma, a frequently lethal form of brain cancer.
Researchers at the Weizmann Institute of Science have developed a system to investigate microglia functions, revealing their role in shaping neuronal networks and contributing to neurodegenerative diseases. The study uses a genetic switch to target microglia cells, shedding new light on their mechanisms of action.
A new sequencing method identified a set of genes used by microglia to sense their environment, called the 'sensome'. As aging increases, microglia's expression of neuroprotective genes becomes more active while toxic actions are downregulated. This discovery may lead to better understanding and treatments for neurodegenerative disorders.
Researchers discovered a defect in microglia's internal recycling program, leading to faulty phagocytosis and accumulation of A-beta protein. This impairment may contribute to the development of Alzheimer's disease by allowing toxic substances to remain in the brain.
A study published in Neural Regeneration Research found that paeonol, a natural compound, attenuates inflammation-mediated neurotoxicity and microglial activation. This suggests that paeonol may be effective in treating neurodegenerative diseases such as Alzheimer's and Parkinson's.
Researchers from LCSB have discovered that microglial cells in the brain produce itaconic acid, an endogenous antibiotic that prevents bacterial growth. This finding has implications for understanding Parkinson's disease and its connection to the immune system.
A study found that Peli1 promotes microglial activation and subsequent inflammatory response in the central nervous system, contributing to autoimmune inflammation. The protein's role in protecting against excessive inflammation was also discovered.
A study published in the journal Neuron reveals that a gene called CD33 contributes to Alzheimer's disease by inhibiting immune cells' ability to remove toxic molecules. Inactivation of CD33 has been shown to enhance microglia's clearance of beta-amyloid plaques, potentially reversing the disease's progression.
Researchers discovered a protective CD33 gene variant that enhances the brain's immune system to clear away toxic A-beta protein, a hallmark of Alzheimer's disease. This finding raises the possibility of using CD33 inhibitors as a potential new approach to treating and preventing Alzheimer's.
A NIH-funded study has discovered a potential strategy for treating Alzheimer's disease by blocking the activity of a little-known regulator protein called CD33. The study found that CD33 promotes late-onset Alzheimer's by preventing support cells from clearing out toxic plaques.
Researchers have identified a structure deviation in microglia cells, allowing for their visualization and behavior study. This breakthrough enables the monitoring of microglia function over time in rats and mice, with potential applications in studying Parkinson's disease and stroke.
Researchers have shed light on microglial cells in Alzheimer's patients, finding they lose two biological functions as the disease progresses. The study suggests beta-amyloid peptides trigger this process, and reversing microglial function could lead to treatments for the disease.
Researchers have discovered a key link between inflammation and Alzheimer's disease progression. The study suggests that drugs targeting IL-1 beta production may provide benefits for patients with Alzheimer's. The findings point to the possibility of developing new treatments by disrupting the production of this pro-inflammatory cytokine.
Researchers find that leakage of fibrinogen into the central nervous system activates immune cells called microglia, leading to nerve damage. Targeting the interaction between fibrinogen and microglia may be an effective alternative for treating multiple sclerosis.
Researchers found that monocytes, a type of immune cell in the blood, can rapidly repopulate the brain after microglia are removed. This discovery highlights a strong homeostatic mechanism to maintain resident immune cells and raises possibilities for delivering therapeutic agents into the diseased brain.
Scientists at Stanford University School of Medicine found that neural stem cells secrete substances that activate microglia, boosting their numbers and strength. This new understanding could improve brain function and lead to the development of therapies for neurodegenerative diseases.
Researchers at Gladstone Institutes discover how a protein deficiency contributes to neurodegenerative disease frontotemporal dementia (FTD). Progranulin prevents microglia from becoming hyperactive, leading to inflammation that destroys neurons and causes debilitating symptoms.
Microglia, the brain's emergency workers, use a long-lasting glutamate-driven calcium wave to detect injuries, allowing them to trace the signal backwards until they reach the site of damage. This discovery could lead to new treatments for conditions such as Alzheimer's and Parkinson's diseases.
Researchers have shown that microglia in the brain target and remove unused connections between brain cells during normal development. The study highlights the newly found importance of the immune system in shaping brain wiring.
A bone marrow transplant has been shown to arrest severe symptoms of Rett syndrome, a devastating neurological disorder, by replacing faulty immune system cells. The procedure significantly extended the lifespan of Rett mouse models and improved their mobility, breathing, and overall health.
Researchers found that honokiol down-regulates pro-inflammatory cytokines and enzymes in microglia via Klf4, a protein regulating DNA. Honokiol also reduces inflammation and neuronal death by targeting Klf4 and pNF-kb.
Research reveals microglia cells prune connections between neurons, shaping brain wiring. The discovery could help understand autism and other neurodevelopmental disorders.
Researchers found that a steroid hormone called ADIOL moderates inflammation in the brain and may lead to new treatments for patients with neurodegenerative conditions. The discovery could also help predict risk or responses to drugs that mimic its actions.
Researchers found caspase enzymes control microglial activation, triggering inflammation and neuronal death in neurodegenerative diseases. Caspase inhibitors showed promise in reducing activated microglia and inflammation in mice.
Researchers found that a naturally present brain chemical signal, CX3CL1, can suppress microglial activation and reduce inflammation in an animal model of Parkinson's disease. This suggests that the communication between neurons and glial cells may play a role in neurodegeneration.
Microglia, immune cells long thought to be dormant, are found to constantly interact with synapses, creating and eliminating them. This discovery challenges current views of the brain and its functions.