Articles tagged with Microglia
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.
Researchers at CU School of Medicine identified microglia's essential role in regulating myelination, a process forming connections between neurons and glial cells. This finding may lead to improved understanding of potential causes for neurological and neuropsychiatric diseases.
Scientists have identified a role for microglia in clearing the extracellular matrix, allowing new synapses to form and improving memory. Disrupting this process can lead to memory problems, including those seen in Alzheimer's and anxiety disorders.
Researchers at the University of Sheffield have discovered a link between defective immune cells and rare childhood brain disorders, such as leukodystrophies. These diseases cause severe physical and mental disabilities in children, with limited treatment options available.
A new study suggests that impairments in microglia play a key role in the development of autism behaviors in some cases. The researchers found that protein overproduction in microglial cells leads to impaired synapse-pruning function, resulting in ASD-like social behavior deficits, primarily in males.
Researchers created a laboratory model of three types of brain cells to study HIV's impact on the central nervous system. The model revealed that HIV infection can take a toll on the brain, causing inflammation and damage. Antiretroviral therapy (ART) can reduce inflammation by around 70%, but also triggers its own unique response.
A study reveals that Alzheimer risk genes are linked to microglia's response to amyloid-beta, a key protein in the disease. The researchers identified 11 new risk genes that are upregulated when facing increased amyloid-beta levels.
Researchers discovered that an immune reaction in the brain adds fuel to the fire of inflammation, leading to the development of Alzheimer's disease. The microglia cells' activation of inflammasomes makes degradation of Aß proteins more difficult, creating a devastating process.
Scientists have identified a specific antibody that binds to brain immune cells and triggers processes that enhance microglia activity. This stimulates the immune cells to detect and degrade abnormal protein deposits, known as plaques, more effectively, potentially providing better protection against Alzheimer's disease.
Researchers found a polymorphism associated with protective effects against major depressive disorder in women. Microglial cells' immune receptors may play a role in neuropsychiatric disorders.
Researchers found that rejuvenating immune cells, specifically microglia, significantly improved brain repair and learning abilities in animal models. This discovery challenges the long-held assumption that microglia drive inflammation after brain injuries.
Visceral fat generates high levels of interleukin-1 beta, over-activating microglia and promoting chronic inflammation. This leads to impaired cognitive function, including difficulties with navigation and learning and memory.
A study published in Nature Communications reveals that microglia can both protect and damage the blood-brain barrier, depending on the level of systemic inflammation. The researchers used fluorescent labeling and two-photon imaging to study the interactions between microglia and the blood-brain barrier.
A preclinical study suggests that targeting overactive immune cells in the brain can limit brain cell loss and reverse cognitive and motor difficulties caused by traumatic brain injury (TBI). Mice treated with an experimental drug recovered markedly better than control mice, showing less tissue loss and improved motor and cognitive per...
New preclinical research suggests that targeting overactive immune cells can improve traumatic brain injury recovery and modulate chronic neurotoxic effects. The study found that a therapeutic strategy to inhibit microglia cells after TBI led to better motor and cognitive performance in mice.
Researchers at RMIT University found that microglia cells can be activated to boost memory performance in rats by up to 50%, reversing damage caused by neuroinflammation. This discovery could lead to the development of new treatments for cognitive decline and dementia.
A recent study has shown that microglia regulate forgetting in the adult brain by weakening and eliminating synapses connecting engram neurons. Inhibiting microglial activity or depleting them prevents forgetting, while intact microglia facilitate the dissociation of engram cells, leading to memory erasure.
Researchers found that microglia, immune cells in the brain and central nervous system, encase macrophages, preventing them from dispersing into areas they shouldn't be. This discovery may lead to new treatments for conditions like multiple sclerosis and Alzheimer's disease.
Researchers at UMass Chan Medical School have developed a gene therapy approach that protects synaptic connections in the brain from damage in multiple sclerosis models. The study suggests that therapies targeting specific circuits of the brain could be effective in preserving vision and preventing neurodegenerative symptoms.
Researchers found that radiation triggers an immune response that severs connections between nerve cells, leading to damage and cognitive problems. The study suggests two potential approaches to prevent this damage: blocking a receptor responsible for synapse removal or tamping down the brain's immune response.
A study by University of Alberta chemists identifies CD33 protein as a factor that may decrease the likelihood of Alzheimer's disease. The most common type of CD33 protein plays a crucial role in modulating microglia function, which can protect against neurodegenerative plaques.
A team of international researchers has identified a potential treatment for reducing brain injury in premature babies by targeting hyperactive microglia with a drug that activates the Wnt signalling pathway. This approach may help protect white matter and prevent long-term memory problems associated with preterm birth.
Researchers found a correlation between dysfunctional microglia and obsessive-compulsive disorder (OCD) behaviors in mice. Female sex hormones exacerbated symptoms, indicating a potential genetic link to anxiety disorders.
New research reveals that immune cells called microglia are active during sleep, rewiring brain connections and repairing damage. Microglia's interaction with neurotransmitters like norepinephrine regulates their activity, suggesting a link between sleep and brain health.
Research in animals shows that chronic stress during pregnancy triggers an immune response in the brain, leading to potential changes in brain functions. The study found that stressed rats showed evidence of neuroinflammation and increased activity levels of microglia, suggesting a link between gestational stress and postpartum depress...
Researchers have made significant breakthroughs in understanding the role of microglia in neuroinflammation, a hallmark of degenerative brain diseases such as Alzheimer's Disease. Studies show that changes in microglial cells can trigger hyperexcitability in the brain, leading to decreased sociability and motivation.
A recent study has identified a key regulator of microglia function during inflammation, which could become a significant component in treating neurodegenerative diseases. TET2 protein modulates the immune response generated by microglia cells in the brain under inflammatory conditions.
A new study found that brain immune cells called microglia drive brain damage in Alzheimer's patients. Eliminating these cells reduces tau-linked brain damage, suggesting a potential therapeutic target.
A study published in the journal Aging Cell found that a lifelong dietary regimen of choline can improve spatial memory and reduce AD-like symptoms in female mice. Choline supplementation also reduces microglia activation, offering protection from brain inflammation and neuronal death.
A new study reveals that APOE4, the strongest genetic risk factor for Alzheimer's disease, impairs the function of human brain immune cells, microglia. This impairment increases inflammation and reduces their ability to remove toxic amyloid from the brain.
Researchers discovered LH dipeptide as a potent anti-inflammatory agent that inhibits the secretion of inflammatory cytokines from microglia, reducing brain inflammation and depression symptoms. Consuming foods rich in LH dipeptide may be a safe method for maintaining good mental health.
A recent Yale study found that high-fat diets stimulate hypothalamic inflammation, leading to changes in microglial cells and regulating energy homeostasis. The research suggests a neurological mechanism controlling food intake, with potential implications for obesity and diseases like Alzheimer's.
Researchers discovered that higher levels of TREM2 protein in cerebrospinal fluid are associated with improved prognosis and reduced cognitive decline in Alzheimer's patients. The study suggests that TREM2 may play a key role in regulating the brain's protective immune response, offering new therapeutic strategies.
Researchers discovered that removing brain immune cells called microglia prevents beta-amyloid plaque formation in rodent models of Alzheimer's. This finding suggests a crucial role for microglia in the disease's development and progression.
Researchers at UCI have developed a mouse model that allows for the study of human brain immune cells in unprecedented detail. The 'chimeric' mouse contains human microglia, enabling the investigation of Alzheimer's mechanisms and potential treatments.
Researchers at Massachusetts General Hospital discovered a key gene interaction that fuels neuroinflammation, leading to cognitive decline and Alzheimer's disease. CD33 and TREM2 genes regulate microglia activity, with CD33 acting as the 'on' switch for inflammation.
The study reveals Galectin-3 plays a key role in regulating immune response associated with Amyloid beta peptide. Researchers have identified genetic mutations linked to increased risk of Alzheimer's, and a potential therapeutic target for blocking galectin-3.
A study has identified a key connection between two damaging proteins in Alzheimer's disease: amyloid beta and tau. Immune cells called microglia may be the missing link between these proteins, which can cause brain tissue damage.
Researchers have developed a microglia-selective fluorogenic probe that triggers fluorescence through gene expression, enabling selective labeling and imaging of microglia cells in live brain tissue. This probe has the potential to detect developing neural diseases such as Alzheimer's disease and stroke.
Researchers found that visual stimulation can prevent neuron degeneration and enhance synaptic function in Alzheimer's disease models. The treatment also improved spatial memory performance in older mice without a predisposition for the disease.
A new study uncovers the presence of 'hidden' microglia in the brain, which show a resemblance to microglia associated with Alzheimer's disease. The researchers hope to find strategies for controlling these immune cells to develop future treatments for neurodegenerative diseases.
Researchers developed a chemical probe that enables live-imaging of microglia in the brain, crucial for understanding brain development and disease. The probe, CDr20, labels microglia in both human- and primate-derived cells, allowing for clinical-relevant studies.
Researchers studied how microglia cells in the brain respond to toxic proteins associated with Alzheimer's disease. The study found that age, sex, and genetics affect microglial response, suggesting that modulating this response could lead to new treatments.
Researchers at Mass Eye and Ear have identified microglia as gatekeepers that orchestrate inflammatory responses in the retina during autoimmune uveitis. By depleting microglia, disease was completely blocked, suggesting a novel therapeutic target for this devastating eye disease.
A new study by University of Notre Dame scientists reveals microglia can cross from the central nervous system (CNS) into the peripheral nervous system (PNS) in response to injury. This finding has broad implications for nervous system diseases and opens up new questions about the function and capabilities of these cells.
A Stanford University School of Medicine study found that blocking a specific protein's activity improved cognitive behavior in aging mice. The researchers identified a gene called CD22, which is involved in microglial phagocytosis and is upregulated with age.
Scientists discovered that microglia, a type of nervous system cell suspected to cause retinal damage, surprisingly had no damaging role during prion disease in mice. Microglia might delay disease progression, providing new insights into inherited photoreceptor degeneration diseases.
Researchers created a high-resolution map of the brain's immune system, showing that all microglia have the same core signature but adapt differently depending on their function. This discovery is significant for understanding brain diseases like multiple sclerosis and Alzheimer's.
A study published in Nature Neuroscience found that individuals with schizophrenia exhibit excessive synaptic pruning, a process normally occurring during adolescence. This abnormality contributes to the development of schizophrenia symptoms.
Researchers at the National Eye Institute discovered that TGF-beta signaling governs immune cell function in the eye, leading to activated microglia and retina damage. Disrupting this signal may represent a potential therapeutic target for treating AMD.
A study published in Nature Neuroscience reveals that defective immune cells in the brain play a key role in Alzheimer's disease. Activating a specific gene, TREM2, can help prevent toxic deposits, but over-activation may have negative consequences.
Researchers at Arizona State University discover that choline supplementation may help fight Alzheimer's disease in mice and their offspring. The study reveals that high choline intake during gestation and lactation improves spatial memory in subsequent generations, suggesting a transgenerational effect.
Research found that activation of microglia in the spinal cord is responsible for increased pain sensitivity in response to stress. Eliminating microglia from the spinal cord prevented these effects, highlighting their role in transmitting pain to the brain.