Articles tagged with Microglia
Inhibiting a key signaling pathway in brain-resident immune cells may calm brain inflammation and slow Alzheimer's disease. The NF-κB pathway's activation triggers inflammatory activation of microglia, leading to tau tangle formation and spread.
A UCI-led study has found that early life adversity can lead to microglia dysfunction, resulting in abnormal stress responses later in life. The researchers discovered that microglial pruning of excitatory synapses during brain development is crucial for refining functional circuits and preventing aberrant stress responses.
A UCI-led study reveals how a TREM2 gene mutation in brain microglia immune cells can increase the risk of Alzheimer's disease. The research found that blocking excess calcium accumulation may be an effective way to modulate microglia behavior and fight the disease.
A study found that microglia's TREM2 receptor is activated up to two decades before Alzheimer's symptoms appear in individuals with a genetic predisposition. This activation may slow cognitive decline and pathological brain changes. The research suggests modulating microglial activity could be a promising therapeutic strategy.
A study found that intact astrocyte networks are essential for neural homeostasis, synaptic plasticity, and spatial cognitive abilities in adult mice. Disrupting these networks impairs spatial learning and memory due to altered neuronal excitability and compromised synaptic transmission.
In a breakthrough discovery, microglia have been found to play a crucial role in forming critical synapses in the brain, particularly in chandelier cells. This finding suggests that immune cells may not only remove unwanted connections but also nurture their formation, which is essential for cognitive functioning.
Researchers found that modulating immune cell activity via TREM2 receptor may impact neurodegenerative disease processes. Hyperactive microglia were shown to retain certain neuroprotective functions, suggesting a potential therapeutic approach.
Prenatal exposure to industrial toxin TCDD may cause long-term damage to brain circuits and potentially lead to neurodevelopmental disorders like autism and ADHD. Researchers found that pharmacological manipulation can restore microglia function, suggesting a possible therapeutic avenue for these disorders.
A new study led by Mount Sinai researchers found that microglia may play a critical role in some cases of brain disease, and provides a comprehensive guide for future studies. The study identified two new genes linked to brain disorders, including Alzheimer's and Parkinson's diseases.
A new study reveals distinct DNA methylation profiles of human microglia cells across different age groups, disease states, and brain regions. The researchers found that interindividual differences in methylation variability had a larger impact than regional or diagnostic differences.
Researchers found that asthma causes immune cells to behave in a way that prevents brain tumor growth, suggesting a potential new therapeutic approach. The findings suggest reprogramming T cells to act like those in asthma patients could be a new treatment for brain tumors.
Researchers from Tokyo Medical and Dental University found that PQBP1 interacts with Tau protein to drive an immune response in the brain. The study reveals a mechanism of inflammation that functions in both viral infection and neurodegenerative disease.
Microglia, the brain's immune cells, migrate to the retina using blood vessels as pathways and require neurogenesis for colonization. The study provides insights into microglial migration and its implications for neurodegenerative diseases.
A team of researchers at Fudan University has found that the protein NeuroD1 does not induce microglia-to-neuron conversion as previously thought. Instead, it causes microglial cell death. The study suggests that this finding may be due to experimental artifacts and highlights the need for stringent evidence in scientific research.
Researchers found that gut microbiome changes can reduce b-amyloid deposits in male mice, indicating a potential target for preventing and treating dementia. Daily fecal matter transplants restored the pre-antibiotic microbiome, suggesting microglia memory plays a role.
A study by Weill Cornell Medicine scientists found that blocking a signaling pathway in brain immune cells can protect against Alzheimer's disease features in a preclinical model. The results suggest a new strategy to block the development of the disease or slow its progression.
New research found that physical activity is linked to lower microglial activation, a key factor in Alzheimer's disease pathology. The study, published in JNeurosci, suggests that exercise may help reduce inflammation and improve cognitive aging in older adults with more severe AD pathology.
A recent study published in Science Advances found that deleting the ABI3 gene increases amyloid-beta plaque accumulation and decreases microglia function, which may contribute to Alzheimer's disease progression. The researchers also identified a link between the mutation and increased risk of late-onset Alzheimer's.
Researchers found that glatiramer acetate improved cognitive behavior and reduced amyloid plaques in a mouse model of Alzheimer's disease. This study suggests therapies targeting the immune system could be effective in treating the disease.
Recent research highlights microglia's involvement in Alzheimer's development and progression. A better understanding of microglial dysfunction may help explore signs and mechanisms of the disease, as well as enable microglia as a potential therapeutic target.
Microglia play a vital support role in maintaining blood vessels in the brain, regulating blood flow and capillary diameter. This discovery may lead to new therapies for diseases affecting small brain vessels, such as Alzheimer's and stroke.
New research reveals that microglia in the brain take up more glucose than previously thought, leading to altered PET scan images. This finding has significant implications for understanding neurodegenerative diseases and developing new diagnostic tools.
A UCL-led research team has identified an anti-viral gene that increases the risk of both Alzheimer's disease and severe Covid-19. The study found that a specific variant of the OAS1 gene amplifies inflammation in the brain, highlighting the importance of the immune system in both conditions.
Researchers at the University of Alabama at Birmingham discovered a small molecule that potently attenuates neuroinflammation in brain and glial cells. This finding presents a promising new approach to treat neurological diseases driven by neuroinflammation, such as stroke, spinal cord injury, and neuropathic pain.
Researchers investigate G-quadruplex stabilization in neurons, astrocytes, and microglia, revealing differences in genomic instability and DNA repair pathways. These findings suggest that stabilized G4s contribute to brain aging and neurodegeneration.
Scientists discovered beige fat cells mediate subcutaneous fat's brain protection and provide anti-inflammatory effects. Beige fat transplantation restored cognitive function in obese mice with dementia-like behavior.
University of Virginia researchers identified a potential avenue for treating seizure-related brain injuries by harnessing the brain's natural immune response. Microglia cells were found to form pouches that tend to swollen dendrites, suggesting a 'healing' process.
Researchers found that early-life inflammation weakens the brain's ability to cope with stress, leading to adolescent depression. Microglial cells overengage with neurons, reducing glutamatergic neuronal activity.
A new study reveals that microglia, the brain's resident immune cells, play a crucial role in regulating brain wiring by sculpting inhibitory neurons. The research showed that microglia interact with GABA-emitting inhibitory synapses through direct physical contact, a process enabled by advanced imaging techniques.
Researchers at IST Austria find that ketamine and 60-hertz light flickering can remove the perineuronal net, a structure responsible for stabilizing brain connections. This could lead to new therapeutic approaches for treating post-traumatic stress disorder and amblyopia.
A study published in Cell Reports has pinpointed a small group of immune cells in the brain that play a crucial role in Alzheimer's disease progression. By targeting these senescent microglia, researchers may be able to slow down disease acceleration and develop new treatment options.
A study published in Nature Aging suggests that low oxygen levels in senile plaques reduce immune system's defensive capacity against Alzheimer's disease. Reduced oxygen supply also compromises microglial activity, leading to increased pathology associated with the disease.
Researchers have shown that microglia play a central role in maintaining normal brain function and can fail to do so, leading to serious brain disorders. This new understanding has the potential to develop better diagnostics and treatments for these diseases.
A team of scientists has found the gene expression signatures underlying microglia associated with amyloid plaque phagocytosis. The findings suggest a new target for interventions to address the underlying disease mechanism of Alzheimer's Disease.
Researchers discovered that phosphorylation of MECP2 protein decreases in brain cells as Alzheimer's disease progresses, while abolishing this phosphorylation enhances neuronal viability and gene expression. The study suggests that modifications of MECP2 could be a therapeutic target for developing specific therapies against AD.
Researchers at University of California San Diego School found that controlling cholesterol in microglia can alleviate chronic pain, a common side effect of chemotherapy. They developed a novel therapeutic approach using a modified version of apoA-I binding protein to reverse the harmful effects of excessive cholesterol.
Researchers found that treating mice with experimental Alzheimer's drugs paired with a treatment to improve brain drainage reduced amyloid deposits more effectively than the anti-amyloid drugs alone.
Researchers at the University of Minnesota identified a new drug target for glioblastoma patients who defy conventional wisdom by surviving beyond expectations. Glioblastoma cells subvert immune system cells called microglia and macrophages, leading to tumor growth.
A new study found no evidence of SARS-CoV-2 virus in COVID-19 patients' brains, despite significant pathological changes and neurological effects. Inflammation triggered by the virus may cause damage to the brain's blood vessels and lead to 'brain fog' in mild cases.
Researchers find that microglia promote the formation of dense-core plaques as part of a defense mechanism, clearing debris from neurons and potentially causing cell death. This discovery suggests that treatments targeting these protective plaques may be more effective than destroying them.
A study by Scripps Research Institute found that experimental antibody therapies for neurodegenerative diseases like Parkinson's and Alzheimer's may cause brain inflammation, potentially eroding their positive effects. The researchers used human brain cells to examine this effect, which was not seen in mouse studies.
Researchers discovered that Niemann-Pick type C disease is associated with neuroinflammation and impaired intracellular lipid transport, leading to the accumulation of lipids in the brain. The findings suggest a potential new approach for monitoring disease progression and response to therapy.
Chronic increases in interleukin (IL)-17A levels in mouse blood reduce microglia activity in the hippocampus, a region crucial for learning and memory. Despite this effect on cognition, spatial memory remains unaffected in mutant mice.
Research reveals microglia's essential role in refining auditory pathways, even when pruning is delayed. Without microglia, connections between neurons don't fully mature, leading to impaired hearing.
Elvira Mass has made a significant contribution to understanding the role of yolk sac-derived macrophages in maintaining healthy organs. Her research found that these cells can self-maintain for a lifetime, producing bioactive molecules and growth factors essential for tissue development.
Research suggests that immune cells in the brain, microglia, contribute to negative mood experienced during inflammation and neurological diseases. Activating these cells can elicit a negative affective state in mice, highlighting their potential link to depression.
Researchers found that maternal immune activation induces sustained changes in fetal microglia motility, contributing to developmental disorders and schizophrenia. Microglial process motility changes remained after birth and were linked to social behavior deficits characteristic of autism spectrum disorders.
Researchers found that microglial surveillance helps maintain normal neuronal activity levels by preventing overactive neurons. This discovery opens new avenues for treating neurological disorders such as Alzheimer's disease, epilepsy, and autism.
Research from the University of Eastern Finland explores the role of diabetes in cellular and molecular changes underlying Alzheimer's disease. Diabetes was found to weaken the accumulation of microglial cells around amyloid plaques and increase the formation of neuritic plaques with prominent tau pathology.
A new study reveals that astrocytes can remove cellular debris from the brain when microglia are impaired. This finding could lead to new therapies accelerating debris clearance and reducing neurodegenerative diseases.
A new study reveals that microglia, immune cells in the brain, regulate behavioral responses by sensing neuronal activation and providing negative feedback. This novel mechanism of neuromodulation has implications for treating neurodegenerative and inflammatory diseases.
A new study found that the PLCG2-P522R genetic variant protects against Alzheimer's disease by enhancing immune cell functions, including phagocytic activity and immune response. The results highlight the importance of targeting this pathway for future therapy development.
PRMT1 controls tissue development and lifespan, as well as stress responses in non-neuronal cells. In neonatal mice lacking PRMT1, severe inflammation is observed, including increased astrogliosis and microglia numbers.
Researchers found that microglia direct neurons to modify their connectivity in response to visual stimuli, shaping the brain's neural circuits. This discovery sheds light on how sensory experience influences brain maturation and may have implications for neurodevelopmental disorders such as autism.
Researchers at Rutgers University are exploring the link between uncontrolled inflammation and microglial cells in the brain, aiming to develop new therapies for neurodegenerative diseases. The team is designing nanomedicines that can target microglia to tamp down inflammation and protect neurons.
Researchers at UVA Health System discovered that many microglial cells originate from blood monocytes, which transform into troops to defend the brain after infant strokes. This finding sheds light on the development of brain's immune defenses and has implications for understanding newborn brain injury.
Researchers developed three techniques to replace malfunctioning microglia, with varying efficiencies and donor sources. The techniques offer promise for treating neurological disorders such as Alzheimer's, ALS, and Parkinson's.
Scientists have identified new points to calm frenzied energy production in the retina, enabling recovery. The excessive byproducts of glycolysis initiate a vicious loop of crosstalk between endothelial cells and microglia, promoting inflammation and dysfunctional blood vessels.
Researchers at UVA School of Medicine discovered that brain defenders called microglia release a unique immune molecule to control the parasite in the brain, preventing symptomatic toxoplasmosis. This finding has implications for brain infections, neurodegenerative diseases and autoimmune disorders.
Researchers discovered brain-resident immune cells that play a crucial role in normal brain development and are essential for the regulation of brain functions. The findings suggest a connection between gut bacteria, white blood cells, and neurological diseases.