Articles tagged with Microglia
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.
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.
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.
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.