Articles tagged with Microglia
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.
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.
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.
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 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.
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.
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.
A recent study published in Journal of Experimental Medicine found that immune cells play a major role in the development of spastic paraplegia type 15. The research, led by Professor Elvira Mass and Dr. Marc Beyer, suggests that severe inflammation in the brain precedes neuronal damage and could be relevant to Alzheimer's disease.
A new study from the University of Oklahoma is targeting cell communication in the hunt for therapies to slow macular degeneration. The research team is studying how cells in the retina communicate and whether the messages they send could be programmed to treat or slow AMD.
Researchers at UC Irvine develop a cell-based platform to deliver disease-fighting proteins throughout the brain, reducing inflammation, preserving neurons, and reversing neurodegeneration in mice. The engineered microglia can detect disease-specific changes and release enzymes to break down toxic proteins.
Calmming the brain's immune cells via norepinephrine may prevent or lessen Alzheimer's inflammation and damage. The study highlights a key role of norepinephrine in mitigating early inflammatory changes and neuronal injury.
Researchers have identified Tim-3 as a promising therapeutic target for Alzheimer's disease by targeting microglia in the brain. Deleting Tim-3 helps kickstart plaque removal, reduce neuroinflammation, and limit cognitive impairment.
A research team has discovered microglia in the peripheral nervous system (PNS) that regulate neuronal soma size throughout evolution. The study challenges long-held beliefs about microglia's absence from the PNS, revealing a common molecular signature and role in regulating neuron size.
Scientists at ISTA create a new brain organoid model that incorporates microglia to study viral infections, such as Rubella, and test the effectiveness of ibuprofen. The results show that microglia play a crucial role in inflammatory reactions and that ibuprofen exerts its protective effects by inhibiting two inflammatory enzymes.
A new study by UCL researchers found that people with visual Alzheimer's disease have a unique distribution of proteins and markers in their brain, leading to symptoms such as reading difficulties. In contrast, those with memory-led Alzheimer's disease have different protein patterns, resulting in symptoms like memory loss.
A research group has uncovered a potential mechanism linking maternal inflammation to delayed neurodevelopment in infants. CD11c-positive microglia, crucial for myelination, play a key role in this process.
A review article reveals CD2AP's crucial role in amyloid metabolism, tau pathology, synaptic function, and neuroinflammation in Alzheimer's disease. CD2AP deficiency accelerates plaque formation, while its loss in neurons leads to reduced spine density and impaired synaptic plasticity.
A new Northwestern University study found that enhancing the brain's immune cells can clear Alzheimer's plaques and restore a healthier brain environment in immunized patient brains. The findings could reshape the future of Alzheimer's treatments by shifting the focus from removing plaques to harnessing the brain's natural defenses.
Researchers at Kyoto University investigated the effects of two-hit stress on mice, finding that it leads to increased microglia activity, neuronal loss, and decreased brain connectivity. Microglia replacement therapy showed promise in rescuing affected mice, with female mice exhibiting higher stress resilience.
Researchers at Kyoto University investigated the effects of two-hit stress on mouse behavior, revealing significant changes in the cerebellum. The study found increased microglia turnover, neuronal loss, and decreased brain connectivity, correlating with anxiety-like behaviors and mental disorders.
A new study reveals that microglia can be reprogrammed from a tumor-promoting state to one that strengthens antitumor responses, reducing brain metastases growth and enhancing immunotherapy responses. Researchers identified a key signaling pathway that, when blocked, reverses the protumoral function of microglia.
Research reveals that micronuclei uptake regulates microglial morphology and gene expression, influencing neurogenesis, neural networks, and cerebrovascular function. This mechanism is crucial for the postnatal brain's development and function.
Scientists from DZNE found that preventing brain inflammation may help treat Alzheimer's disease. The study, published in Immunity, suggests that inhibiting the NLRP3 inflammasome can reduce neuroinflammation and help microglia clear harmful amyloid-beta deposits.
Dr. Mikael Simons is being recognized for his pioneering research on myelin biology, glial cell biology, and neuroinflammation that continues to inform MS research. His work has helped identify a promising therapeutic target with potential to benefit people with MS.
Researchers have found that microglia function differently in adult male versus female mice when given an enzyme inhibitor, with potential broad implications for how neurological diseases are studied. This discovery highlights the necessity of gender-specific research and may lead to new disease-modifying therapies targeting microglia.
The study provides insights into the roles of microglia in neurodegenerative diseases, revealing nine transcriptionally distinct subpopulations. The GPNMB-high Lipo.DAM signature is associated with Alzheimer's Disease and Multiple Sclerosis, and may hold relevance for immune-based therapies.
Researchers explore the role of efferocytosis in reducing inflammation and containing injury spread after an ischemic stroke. Efferocytosis may offer a promising therapeutic strategy to promote neural regeneration and minimize brain damage.
Researchers have unveiled a critical mechanism linking cellular stress in the brain to Alzheimer's disease progression, highlighting microglia as central players in both protective and harmful responses. The study reveals that blocking a specific stress pathway reverses symptoms of Alzheimer's disease in preclinical models.
Ocular immune-related diseases, including uveitis, diabetic retinopathy, age-related macular degeneration, and Graves' ophthalmopathy, are caused by abnormal immune inflammatory responses. The review highlights the role of microglia and other macrophages in these conditions, providing new target cells for prevention and treatment.
Researchers found that microglia clear amyloid-β plaques from the brain before plaque formation and may cause more plaques when homeostatic. In contrast, activated microglia help compact plaques in neurons, offering a protective role.
Researchers have developed a network-based approach to understand how immune cells called microglia transform and drive harmful processes like neuroinflammation in Alzheimer's disease. The study identified three unique subtypes of harmful microglia that promote disease progression, with genetic signatures driving their behaviors.
Researchers uncover the significance of neuroinflammation in Niemann-Pick type C disease, a rare form of childhood dementia. They identify translocator protein (TSPO) as a potential biomarker for disease monitoring and response to therapy.
Researchers at Texas A&M University College of Medicine have developed a nasal spray treatment using stem cell-derived vesicles that reduces inflammation and plaque buildup in the brain, delaying Alzheimer's disease progression. The treatment targets microglia cells, which become harmful over time, leading to progressive neuron loss.
Chronic neuroinflammation, driven by activated microglia and astrocytes, is a hallmark of neurodegenerative diseases. Targeted therapies that modulate microglial and astrocytic activity show promise in mitigating neuroinflammation.