Articles tagged with Microglia
Research by Tohoku University scientists found that contextual fear conditioning alters genes associated with the synapse in microglia, indicating a new mechanism linking microglia and neuronal activity related to fear conditioning. This non-immune communication may play a key role in fear memory consolidation and extinction.
A newly developed agonistic antibody targeting TREM2 reduced amyloid burden and alleviated cognitive decline in mice with Alzheimer's disease. The study suggests that increasing TREM2 activation could have therapeutic effects such as improved cognition.
A new study published in Development Cell shows that microglial cells develop in a unique wave-like pattern throughout human brain development. The research, led by Professor Diego Gomez-Nicola, used post-mortem human brain samples to create the largest-ever study on microglial development across the human lifespan.
Researchers successfully developed artificial replicas of GPCRs, allowing for controlled activation and replication of original functionality. The method enables precise modulation of immune cells' responses, holding promise for treating diseases targeted by GPCRs.
Researchers at UC San Francisco have discovered how to shift damaged brain cells from a diseased state into a healthy one using CRISPR technology. The study found that reprogramming microglia cells can help remove protein plaques and protect synapses, potentially treating Alzheimer's and other forms of dementia.
A new study published in Nature reveals that microglia cells change their molecular state to match neighboring neurons, influencing neural circuit function. The researchers found that different types of cortical neurons recruit specific numbers of microglia, which then adapt to the neuron's environment.
A team of researchers from The Mount Sinai Hospital has made a groundbreaking discovery into the genetic and molecular mechanisms that predispose individuals to Alzheimer's disease. They identified 21 candidate risk genes, including SPI1, which regulates microglia and AD risk.
Microglia that express the APOE4 gene cannot metabolize lipids normally, leading to a buildup of excess lipids that interferes with nearby neurons' ability to communicate. Restoring normal lipid metabolism in microglia may help treat some symptoms of Alzheimer's disease.
A new study reveals that air pollution and maternal stress during pregnancy can lead to altered brain development and social behavior in male mice, exhibiting autism-like traits. In contrast, female mice are not affected by these environmental factors.
Timothy Huang has been awarded $2.8 million by the National Institute on Aging to study the SORLA gene and its link to Alzheimer's disease. The project will use human stem cells transplanted into mice to determine how specific mutations impact microglia function.
A multi-site trial found OP-101 to be effective in reducing inflammatory markers and markers of neurological injury, with improved outcomes for patients. The study showed a significant reduction in the composite outcome of mechanical ventilation or death at 30 and 60 days after treatment.
Researchers have discovered that lymphatics, which remove waste from the body, also help seed early brain cells in zebrafish. The study found that precursor cells expressing a specific gene migrate to the brain via lymphatic vessels, highlighting the importance of these vessels in microglia development and brain function.
Studies suggest a link between Fusobacterium nucleatum and Alzheimer's disease, with the bacteria generating systemic inflammation and exacerbating symptoms. Targeting the bacteria could slow periodontal disease progression and potentially slow Alzheimer's progression as well.
In a new study, researchers found that microglia cells are responsible for neuronal death in a mitochondrial disease mouse model. Suppressing these cells with the drug Pexidartinib increased life expectancy and reduced motor problems. Further research is needed to understand the specific process by which microglia attack neurons.
Researchers at UT Health San Antonio found that rapamycin causes an increase in beta-amyloid protein plaques in mouse models, contradicting its potential benefits. However, a novel method to decrease plaques was discovered by deleting the Tsc1 gene from microglia, leading to increased Trem2 levels and decreased plaques.
Researchers at Karolinska Institutet have successfully repurposed a cancer drug to target neuroinflammatory diseases like multiple sclerosis. A novel drug carrier was developed to deliver the treatment specifically to microglia, reducing inflammation and disease progression.
A study by Kyushu University researchers has analyzed the development and genetic profile of a set of cells that construct the brain's immune system. The findings reveal that meningeal macrophages develop in the same way as other microglia, but perivascular macrophages originate from meningeal macrophages after birth.
A Johns Hopkins Medicine study found that a protein called STING responds to clean-up signals in brain cells damaged by Parkinson’s disease by creating a cycle of inflammation that accelerates the disease’s progression. In mice with deactivated STING proteins, there was less microglial activity and brain cell death.
A new study suggests that supplementing a diet with Ascidiacea, also known as sea squirts, reverses some main signs of aging in animal models. The researchers found that plasmalogens, vital to body processes, decrease with age and contribute to neurodegenerative diseases like Alzheimer's and Parkinson's.
A new study in mice suggests that forcing the turnover of specific immune cells called microglia can reverse cognitive and behavior problems associated with concussions. The findings provide a potential pathway for developing post-concussion therapies to ward off long-term mental health issues.
A new study found that microglia regulate neuronal subtypes differently in response to bacteria, affecting intrinsic excitability. Pyramidal cells exhibited lower excitability, while Purkinje cells showed higher excitability when modulated by 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.
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 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.
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.
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 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.
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.