Articles tagged with Microglia
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.
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.
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.
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.
Researchers discovered that microglia cells are constantly active and create and eliminate synapses, contributing to learning and memory. Microglia appear to be involved in creating or changing the extracellular space around synapses, affecting brain signaling.
A team of international scientists led by Dr Florent Ginhoux have uncovered the origins of microglia, white blood cells specific to the brain, revealing they derive from a particular structure in the mouse embryo. This understanding may lead to new strategies to manipulate microglia for treating various brain disorders.
A diet rich in luteolin reduces inflammation in the brain and related memory deficits. Luteolin improves cognitive health by acting on microglial cells to reduce inflammatory cytokine production.
Researchers have discovered a direct relationship between a psychiatric disorder and the immune system, specifically microglia cells derived from bone marrow. Bone marrow transplants cured mutant mice with compulsive hair-pulling behavior, suggesting potential new treatments for obsessive-compulsive disorder.
Research suggests that microglia, immune cells in the brain, play a significant role in neuron loss during Alzheimer's disease. Stressed nerve cells secrete chemical messengers that attract microglia, leading to inflammation and elimination of neurons.
Scientists at Lund University successfully injected nanowires into rat brains, revealing that the brain's 'clean-up' cells (microglia) take care of the wires. After 12 weeks, only minor differences were observed between test and control groups.
Researchers at Mayo Clinic found that inflammation in the brain helps clear amyloid deposits, contradicting long-standing scientific belief. The study suggests that manipulating brain inflammation could be a potential therapeutic approach to treat Alzheimer's disease.
Researchers discover that activating brain immune cells with IL-6 leads to clearance of amyloid plaques, suggesting a new therapeutic approach for Alzheimer's disease. This breakthrough discovery may lead to a treatment that removes these hallmark disease-causing structures from patients' brains.
Researchers discovered that glioma cells use microglia, the brain's immune cells, to grow and expand rapidly. By manipulating microglial cells' receptors, gliomas can clear the way for further growth.
Researchers studied microglial cells in mouse retina to understand their response to neurodegenerative processes. Their work may aid in the development of therapeutic strategies for Parkinson's and Alzheimer's diseases.
Researchers found a direct link between smoking and brain damage due to NNK, a tobacco compound that provokes white blood cells to attack healthy brain cells. This can lead to neuroinflammation, conditions like Multiple Sclerosis. NNK is present in all forms of tobacco, also affecting second-hand smokers.
Researchers found that microglial cell degeneration contributes to loss of neurons and dementia, contradicting the popular neuro-inflammation theory. The study suggests that anti-inflammatory drugs may not be effective in fighting dementia.
A study by University of California, San Diego researchers identified a protein called Nurr1 that protects neurons from excessive inflammation, which can lead to neurodegenerative disorders like Parkinson's disease. The protein's protective function was found to involve shutting off inflammatory responses in microglia and astrocytes.
Researchers found that a gene called Nurr1 limits pro-inflammatory neurotoxic mediators in microglia and astrocytes, suggesting a link between inflammation and Parkinson's disease progression. The study may point to new avenues for therapy and anti-inflammatory treatments to combat the disease.
Scientists at Emory University School of Medicine have found a way to block the toxic effects of tPA, a life-saving clot-busting drug used in acute stroke treatment. By blocking LRP1, a molecule that transmits inflammation signals triggered by tPA, the researchers were able to soften the drug's impact on the brain.
Research suggests that cerebral inflammation and microglia activation contribute to schizophrenia development. Anti-inflammatory agents targeting activated microglia may provide a new treatment option for the condition.
Scientists at Georgetown University Medical Center identified a new way to limit brain cell damage by reducing microglial activation. They found that a selective activator of a key receptor can turn off microglial activity, potentially treating conditions like stroke, Alzheimer's disease, and Parkinson's disease.
Researchers discovered that luteolin, a plant flavonoid found in celery and green peppers, can disrupt the inflammatory response in the brain. The study found that luteolin significantly reduced inflammation by inhibiting the production of interleukin-6 (IL-6) in microglial cells and mice.
Researchers discovered a protein made by microglia that helps accelerate tumor growth, and are looking for others. The findings have implications for both genetic and sporadic brain tumors.
A fibrous protein called fibrinogen promotes multiple sclerosis (MS) when it leaks into the brain, triggering inflammation. Researchers at UCSD have identified a specific receptor that binds to fibrinogen and inhibit this inflammation process.
Researchers have successfully treated mice with gene therapy, reversing neurological damage and deficits caused by the genetic defect that leads to metachromatic leukodystrophy. The treatment involves using hematopoietic stem progenitor cells genetically modified to express high levels of ARSA protein.
Researchers at Case Western Reserve University have found a protein associated with brain cell death in Alzheimer's disease. The study suggests that the multi-domain protein Vav plays a critical role in triggering a cascade of reactions leading to oxidative damage and neural cell death, a key characteristic of Alzheimer's.
Research findings clarify microglia's induction and blockage of oligodendrogenesis in MS, shedding light on disease mechanisms. The study highlights the complex interplay between microglial activation and oligodendrogenesis in MS.
Researchers say cannabidiol, a compound found in marijuana, may protect the eye from growing leaky blood vessels and prevent diabetic retinopathy. Early studies indicate it works as an antioxidant to neutralize toxic superoxides and inhibit destructive systems.
Researchers at Canadian Institutes of Health Research find that bone marrow-derived microglia can efficiently destroy amyloid plaques, the hallmark of Alzheimer's disease. The discovery provides new hope for patients by highlighting a potential therapeutic approach to curbing plaque development and prolonging autonomy.
Microglia have been found to play a crucial role in neuropathic pain by releasing Brain-Derived Neurotropic Factor (BDNF). BDNF disrupts inhibition in the spinal cord, leading to abnormal pain signals. The discovery offers new hope for diagnostics and treatment of chronic pain.
Researchers found that resveratrol can prevent amyloid beta from killing neurons by blocking a key protein called NF-kB in microglia. This discovery singles out resveratrol as a promising therapeutic intervention for Alzheimer's disease.
Researchers found that older animals exhibited an exaggerated inflammatory response in the brain compared to younger adults when exposed to a peripheral infection. This led to prolonged sickness symptoms and cognitive disorders. The study suggests that normal aging may also prime microglial cells, making them overreact to infections.
A recent study published in Diabetes journal found that minocycline limits retinal damage caused by microglia cells in diabetic rats. The antibiotic reduces neuroinflammation and activation of microglia, resulting in less nerve cell death and improved vision outcomes.
Microglial cells are highly dynamic, constantly sampling their environment and interacting with neurons. In response to cerebral hemorrhage, microglial cells rapidly rush to the injured site, shielding it and decomposing damaged tissue.
A new study suggests that nicotine may protect the brain by inhibiting the activation of microglia, a key step in nerve cell death. The researchers identified the alpha-7 acetylcholine receptor subtype as the specific site where nicotine binds to block microglial activation.
Researchers at Case Western Reserve University discovered molecules that play a critical role in triggering inflammation in the brain, which speeds up Alzheimer's disease progression. The study found that blocking these molecules' interaction with amyloid plaques could lead to a slower disease progression.
Researchers found a specific protein, OX2, that controls inflammation in the brain. OX2 deficiency may lead to chronic brain inflammation, associated with Alzheimer's disease, multiple sclerosis, and AIDS-related dementia.