Articles tagged with Microglia
A new study by UC Berkeley researchers suggests that hyperreactive astrocytes are a primary driver of childhood epilepsy, particularly in the inherited disorder tuberous sclerosis complex. The findings highlight possible therapies to reduce inflammation and alleviate seizures, challenging the traditional view that neurons are the sole ...
A new study by UC Riverside scientists has identified MAPK14, a brain protein, as the driving force behind neuroHIV damage, which causes dementia, neuropathy, and memory problems. By targeting this protein, researchers hope to develop a treatment for neuroHIV, a condition affecting millions worldwide.
Scientists at Salk Institute create first microprotein atlas of human frontal cortex with and without Alzheimer's disease, identifying 1,067 new microproteins and a potential link to immune cell dysfunction in Alzheimer's. The atlas provides a system for investigating microproteins in aging and neurodegeneration, bringing scientists cl...
Researchers from Fudan University developed a strategy to achieve efficient engraftment of macrophages in peripheral organs using Mr BMT, a technique that replaces microglia in the CNS. The study shows that Mr BMT preserves tissue homeostasis and innate immune response, with durable macrophage replacement lasting at least 9 months.
Salk Institute researchers found microglia's novel way to contribute to ALS progression and death, using TAM receptors to find and kill motor neurons in spinal cords of mice with ALS. The study suggests a new target for therapy innovation, but notes the complexity of variables involved.
Microglial cells from patients with genetic and sporadic frontotemporal dementia differ in function and gene expression. Changes in lysosomal function and gene expression profiles are observed, suggesting a common factor in disease processes.
Researchers identified TIMP2 as a key factor supporting healthy microglial function in the aging brain. Restoring TIMP2 in aged mice improved microglia's ability to clear debris and reduced inflammation, suggesting potential therapeutic strategies for neurodegenerative disorders.
Researchers at UC San Diego identified a key cellular pathway that drives brain degeneration in both Sanfilippo syndrome type A and Alzheimer's disease. The study reveals how the brain's immune cells respond to waste buildup, providing a novel target for drug development.
Researchers identified a protective subtype of microglia that expands as Alzheimer's disease progresses, playing a key role in clearing harmful material from the brain. The study provides insights into how the brain's immune cells change across the lifespan and throughout Alzheimer's disease, paving the way for therapies that strengthe...
Researchers found specialized astrocytes in mouse brains that can repopulate damaged areas and rebuild cells. These 'regenerative' astrocytes send newly formed cell nuclei to the site of injury, knitting the network back together.
Researchers at Stanford University discovered that aging brings a large influx of immune cells into the brain, upending previous assumptions about the brain's immune system. The study suggests that these immune cells may interact with the brain and contribute to its resilience against Alzheimer's disease.
Researchers found that female mice's microglia form prolonged contacts with neurons during recovery, leading to synaptic remodeling and plasticity. This phenomenon was not observed in male mice, highlighting differences in brain recovery processes between sexes.
Human microglia mature slowly compared to other animals, influencing cognitive abilities and enabling powerful brain functions. The discovery sheds light on what made the human brain unique during evolution.
A study found that brain immune cells undergo substantial remodeling in midlife, leading to chronic neuroinflammation and potential dementia risk. The research used advanced single-cell analysis techniques to analyze postmortem hippocampal tissue from 40 healthy adults.
Researchers discovered that reducing microglial activity worsened abnormal electrical activity and increased seizure-like events in a mouse model of Alzheimer's disease. Microglia are not just drivers of inflammation but also perform important housekeeping functions to maintain healthy brain activity.
Researchers found that aged mice brains show increased micronuclei, which microglia internalize, leading to changes in morphology and gene expression. This process may contribute to age-associated inflammation and vascular dysfunction.
Researchers identified ZFP384 as a key factor in diminishing microglial reparative functions after stroke. By blocking ZFP384, the study found that microglia retained their reparative properties, leading to enhanced remyelination and synaptic plasticity, and improved long-term neurological function.
A study published in Nature Neuroscience reveals that the TDP-43 protein plays a crucial role in regulating microglial function. Microglia lacking this protein develop motor impairments and exhibit structural alterations in brain regions, highlighting its importance in preventing neurodegenerative diseases.
A new study reveals ATOX1 as a key regulator of oxidative stress, neuroinflammation, and microglial survival in Alzheimer's disease. ATOX1 expression is downregulated in microglia associated with Aβ plaques, leading to copper accumulation and cellular toxicity.
Researchers have identified an experimental molecule called OLE that can restore part of the brain's protective function against Alzheimer's disease. The compound helps microglia enclose and contain beta-amyloid plaques, reducing their size and toxicity.
Researchers identified age-related genetic changes in microglia that may drive inflammation and neurodegeneration in Alzheimer's disease. Cancer-associated mutations were found in genes commonly linked to clonal hematopoiesis, promoting inflammatory activity.
A study published in Communications Biology found that lysophosphatidic acid (LPA) exacerbates chronic pain and drives mirror-image pain after a stroke. The researchers used imaging mass spectrometry to visualize LPA and other molecules, revealing a sequential pathological process that leads to bilateral pain.
Researchers have identified an experimental molecule called OLE that helps restore microglia's protective function against Alzheimer's disease. The compound reduces beta-amyloid plaque size and toxicity, improving cognitive performance in memory tests.
A study published in Translational Psychiatry suggests that low-dose minocycline may help treat panic disorder by reducing inflammation in brain cells. The antibiotic was found to have a similar effect to the commonly prescribed medication clonazepam, with lower doses required to achieve similar results.
Researchers at DZNE discovered complex, situation-dependent interactions between glioblastoma cells and microglia in the brain. The study found that microglial activity changes as tumors spread, influencing containment and spread of the disease.
Researchers identify calcium as a key chemical signal that triggers immune cells during obsessive-compulsive and anxiety-related behaviors. This discovery establishes a new framework to study how anxiety arises and persists through calcium signals in microglia, potentially leading to targeted therapies.
Researchers discover cancer-driving genes in microglia of Alzheimer's patients, suggesting a link between blood cancers and the neurodegenerative disease. The findings could lead to new diagnostic tools and therapeutic options for Alzheimer's.
Research suggests that persistent pain drives progressive changes in the hippocampus, a brain region involved in emotional regulation. This can shape whether people develop depression or remain emotionally resilient. The study's findings challenge the idea that depression is an inevitable consequence of long-term pain.
A study published in Science reveals that microglia and the protein RANK are involved in regulating the hypothalamic-pituitary-gonadal axis, which controls fertility. The research found that suppressing RANK expression led to distorted reproductive function, including reduced sex hormones and hypogonadism.
A new study reveals that astrocytes actively participate in motor-learning circuit rewiring by eliminating synapses in the striatum. The research identifies MEGF10 as a key molecular mediator of this process, which is regulated by dopamine signaling and neural activity.
A UT Health San Antonio researcher will study how microglia contribute to the spread of toxic tau protein in Alzheimer's disease. The study aims to clarify whether microglia act as barriers or accelerators in the cascade of the disease, potentially leading to new treatments.
A new study suggests that a lack of fiber in the diet may impair emotional memory in older adults, linked to cognitive problems and inflammation. The amygdala, responsible for processing fearful experiences, is sensitive to highly processed diets, regardless of fat or sugar content.
A large-scale Japanese cohort study and mouse experiments reveal that maternal perinatal depression increases autistic-related traits in toddlers, with a particularly strong impact on girls. The findings suggest a sex-specific neurobiological pathway underlying these effects.
A study led by Cold Spring Harbor Laboratory researchers found that inhibiting the protein PTP1B improves learning and memory in an Alzheimer's disease mouse model. This suggests that PTP1B inhibition can also improve microglial function, clearing up Aβ plaques.
Researchers found that inhibiting microglia activity improved young mice's recall of fearful experiences. Microglia markers were also increased in brain areas related to memory formation, suggesting enhanced memory recall. This study may provide insight into preventing infantile amnesia and understanding human memory loss.
Scientists found that blocking microglia prevents infant forgetting and improves memory in mice, suggesting a role for microglia in memory formation. Microglia inhibition also enhances engram cell activation, providing a functional explanation for enhanced memory recall.
Research found that prolonged heavy drinking induces neuroinflammation, promoting negative emotional states lasting for weeks into abstinence. Inhibiting proinflammatory microglia activation during alcohol exposure blocks the development of anxiety and fear memory.
A Northwestern University study found an injectable regenerative nanomaterial helps protect the brain during a vulnerable window after most common type of stroke. The therapy successfully crossed the blood-brain barrier and reduced brain damage, showing no signs of side effects.
Researchers discovered that female brain immune cells called microglia express more interferon-related genes when responding to amyloid-β plaques, causing more harm to neuronal connections. This finding suggests a potential sex-specific treatment approach for Alzheimer's disease.
Researchers have identified two proteins that allow cancer cells to evade destruction by brain immune cells, known as microglia. By removing these proteins, microglia play a key role in eliminating cancer cells during the early stage of their arrival in the brain.
Researchers successfully used microglia replacement to halt a fatal neurological disease in human patients, marking a significant advancement from initial mouse model success. The approach has evolved into an efficient and clinical meaningful strategy, with potential applications across neurological diseases.
Researchers from UT Health San Antonio discovered that changes in brain fats play a major role in Alzheimer's development and progression. Targeting microglia, the brain's immune cells, may help restore balance and support brain health. Progranulin levels also emerged as a key lipid regulator.
Researchers have identified two groups of brain cells in mice that regulate anxiety - a 'gas pedal' that accelerates anxiety and a 'brake pedal' that prevents it. The discovery could lead to the development of new therapies for anxiety disorders by targeting these microglia.
Researchers identified a PU.1-promoting subset of microglia that suppresses inflammation and protects cognitive function in mice with Alzheimer's disease. This discovery opens a new avenue for immunotherapies targeting microglial activity.
Researchers have identified a distinct population of neuroprotective microglia that may point to a new therapeutic approach for Alzheimer's disease. Microglia with reduced expression of PU.1 and co-expression of CD28 limit neuroinflammation and slow amyloid plaque build-up.
Alzheimer's disease disrupts the daily activity patterns of brain cells involved in removing amyloid plaques, suggesting a potential therapeutic target for treating the disease. Controlling these circadian rhythms could help prevent disease progression.
Researchers discovered a gain-of-function mutation in the TREM2 gene that impairs microglial function and increases risk for Alzheimer's disease. The study found that female mice with the T96K mutation had reduced microglial activity, leading to increased amyloid beta accumulation.
A new technology allows for clear observation of living retina and microglia's behavior, revealing their increased activity before tissue damage in diabetic mice. The study found that the diabetes drug liraglutide reduced microglia's activity in healthy mice too, suggesting a direct modulation mechanism.
Researchers discovered elevated TSPO levels in the brain of genetically engineered mouse models and human patients with familial Alzheimer's disease, indicating a potential biomarker for early detection. The study aims to explore how blocking or enhancing TSPO could halt disease progression.
Researchers have discovered that microglia, the brain's immune cells, play a key role in how the brain adapts during adolescence. This understanding may transform how neurodevelopmental disorders are treated during this window and possibly into adulthood. The study also found that microglial contact with axons increases dopaminergic ci...
Research reveals neuroglia play active role in brain function, driving disease progression through atrophy and functional decline. Therapeutic strategies targeting neuroglial signaling may prevent damage following brain injury or protect against neurodegenerative processes.
Researchers at Stanford Medicine developed a way to replace more than half of the most severely affected brain cells with non-genetically matched precursor cells in mice. The approach helped animals live longer and reduced behavioral symptoms of the disease, offering hope for families of children with these rare diseases.
The JAK2-STAT3 pathway contributes to inflammation and injury after ischemic stroke. Targeting this pathway shows promise for reducing brain swelling, neuronal death, and improving recovery. Several inhibitors have been found effective in preclinical models, including Tyrphostin AG490, Ruxolitinib, and natural compounds like genistein.
UCSF scientists identified a receptor that enables microglia to engulf and digest amyloid beta plaques, leading to fewer and smaller clumps. This discovery creates an opportunity for new therapies targeting the receptor ADGRG1.
In a breakthrough study, researchers at the University of Rochester Medical Center found that microglia cells respond differently than neutrophils to photoreceptor damage in the retina. This discovery has high implications for treating vision loss caused by photoreceptor cell damage.
A new treatment method using microglia replacement has shown promising results in halting the progression of genetic neurological disease ALSP in both mice and human individuals. The treatment, developed at Fudan University, successfully replaced mutated microglia with healthy ones, improving neurological function and extending life ex...
Researchers at Harvard University's Wyss Institute have successfully created human microglia cells in a dish, using induced pluripotent stem cells, within four days. This breakthrough enables new avenues for brain disease-focused research and potential therapeutic perspectives.
Researchers found that aging increases the brain's vulnerability to low oxygen levels, disrupting the blood-brain barrier and leading to inflammation and cognitive decline. The study identified specific oxygen levels that trigger BBB disruption, with older mice showing increased sensitivity even at mild hypoxic levels.
University of Oklahoma researchers discovered ZIP4 protein drives glioblastoma progression through extracellular vesicles and reprogrammed microglial plasticity. The study identifies ZIP4 and TREM1 as promising therapeutic targets for treating aggressive brain cancer.
Researchers at Vrije Universiteit Brussel have made a significant discovery in replacing faulty microglia with monocytes, opening up new avenues for future therapies. However, the new cells may not fully replicate the normal functions of microglia, highlighting the need for further improvement.