Articles tagged with Microglia
Researchers at Gladstone Institutes discovered that blood leaking into the brain triggers toxic genes in microglia, turning them into harmful cells that destroy neurons. Fibrin, a blood protein, is responsible for this process, which can lead to cognitive dysfunction and motor impairment.
Researchers at the University of Utah Health have made a groundbreaking discovery about the role of microglia in controlling anxiety-related behaviors. The study found that specific microglia populations activate anxiety behaviors while others dampen them, and these cells communicate with neurons to invoke behaviors.
A recent study found that a unique subset of microglia, ARG1+, plays a crucial role in cognitive functions and development. This discovery could lead to new therapeutic approaches for Alzheimer's disease, schizophrenia, and depression. Female animals exhibited more pronounced behavioral impairments caused by ARG1 microglial deficiency.
Researchers create a human-brain-like environment to study microglia development and function for the first time in living human-derived tissue. The findings suggest that brain environment influences microglia development and function, particularly in diseases such as autism spectrum disorder and Alzheimer's disease.
A study published in Stroke identified two proteins, R-spondin 3 (RSPO3) and LGR4, that trigger a signaling pathway to reduce inflammation and promote neurite outgrowth in the ischemic brain. This discovery provides new hope for patients with ischemic stroke by targeting RSPO3/LGR4 signaling.
Anzela Niraula won the 2023 Endocrine Images Art Competition with her image of microglia mandala, highlighting its significance in endocrine research and obesity pathogenesis. The prize includes complimentary registration to ENDO 2023 or 2024.
KNT-127 exhibits anti-stressing and anti-depressant effects in mice, improving social interaction and reducing stress-induced hormone levels. The agent suppresses neuronal inflammation and newborn death without affecting neurogenesis.
Scientists are investigating how brain immune cells called microglia change shape in response to hazards using gene transcripts as molecular mediators. The goal is to gain insights into the mechanisms involved and potentially develop new therapies for neurodegenerative diseases.
Researchers at UVA Health System have made a breakthrough discovery about the role of microglia in seizure disorders. The study suggests that enhancing microglial activity could be a promising approach to preventing and managing seizures, offering new hope for patients who don't respond to existing treatments.
A repurposed HIV drug has been found to restore the brain's autophagy function, helping prevent build-up of misfolded proteins and slowing disease progression in mouse models of Huntington's disease and dementia. This discovery provides clues to how this process could be slowed or prevented in humans.
Targeting a specific antiviral pathway may one day offer a new way to treat or delay cognitive decline in Alzheimer's and frontotemporal dementia. Researchers found that inhibiting a key enzyme called cGAS can help neurons become resilient to tau protein buildup, a hallmark of these diseases.
Researchers have found a new target and drug combination that appears to stop the destruction of vision in premature newborns. By blocking ACAT1, an enzyme that converts cholesterol into smaller pieces, scientists can prevent the formation of leaky blood vessels and inflammation in the retina.
A new study at Umeå University reveals that tick-borne encephalitis virus infects distinct brain cell types and regions depending on the immune system's activation status. The researchers mapped the virus's behavior in the brain, identifying specific areas and cells infected by TBE virus.
Researchers at Nagoya University found an alternative route for microglia colonization in the embryonic brain, suggesting a novel approach to combat diseases like fetal brain dysfunction. Macrophages can convert into microglia later in development, providing new insights into microglial plasticity and behavior.
Researchers found that traumatic brain injury suppresses the recycling function of both neurons and immune cells, including microglia and white blood cells. Boosting this process with a drug like rapamycin improves recovery in mice, reducing inflammation and enhancing memory function.
A recent Brazilian study found that the Spike protein from SARS-CoV-2 is implicated in post-COVID-19 memory loss, with researchers identifying TLR4 receptor as a potential therapeutic target. The study involved experiments with mice and showed that infusion of the Spike protein induced delayed memory impairment.
Researchers developed HIV-1-infection models in human microglia cell cultures to investigate the insertion of the HIV-1 genome. They discovered a correlation between a cellular chromatin factor and the sleeping virus phenotype, linking viral integration to topologically associated domains.
Researchers at NTU Singapore have found a way to spur brain immune cells to clear toxic waste linked to Alzheimer’s disease by targeting their metabolism. The study reveals a ‘metabolic switch’ in the brain’s immune cells that can be manipulated to improve their function.
Researchers have found a possible new target for therapies aimed at treating age-related neurological diseases by linking increased presence of immune cells to conditions like Alzheimer's disease. Microglia, specialized immune cells in the brain, can adopt a dysfunctional state that contributes to neurodegenerative diseases.
A study by Washington University School of Medicine suggests targeting T cells to prevent neurodegeneration and treat Alzheimer's disease. The research indicates that microglia partner with T cells to cause brain damage in the disease, and blocking their entry can avoid most neurodegeneration.
Researchers identified microglia as key players in chemo brain inflammation, suggesting a potential target for treatment. In a mouse study, deleting microglia restored memory and lowered brain inflammation after paclitaxel treatment.
Researchers found that immune cells play a key role in hypertension, weakening blood vessel walls and damaging the blood-brain barrier. Inhibiting inflammatory messengers may be a new therapeutic target for treating hypertension.
Researchers found that gene therapy approach and small molecule treatment can calm the destructive cells of ALS by preserving upper motor neurons. Improving mitochondrial health also reduces astrocyte attack on diseased neurons, offering new hope for treating ALS.
Researchers found that platelet depletion increased amyloid plaque size and neuronal damage in APP-PS1 mice. However, platelets may have a beneficial role in limiting plaque growth and attenuating neuritic dystrophy at advanced stages of Alzheimer's disease.
Neuroscientists have found a way to safely insert healthy new immune cells into the brain, vaulting a key hurdle in treating neurodegenerative diseases. By making donor microglia resistant to the drug pexidartinib, they can potentially harness microglia to treat diseases such as Alzheimer's and Krabbe disease.
A team of researchers led by Adrian Oblak and Peter Bor-Chian Lin studied the INPP5D gene, which is associated with microglia-specific immune cells. They found that reducing its expression can mitigate Alzheimer's disease pathology, preserving cognitive function in lab models.
Researchers discovered a modified form of an inflammatory immune protein called complement C3 that is present at higher levels in women's brains with Alzheimer's compared to men's. This finding may explain why women are more likely to develop the disease, as estrogen levels drop during menopause and lose their brain-protective effects.
Researchers identify INPP5D as a key player in the inflammation process contributing to Alzheimer's disease, which may offer new potential targets for therapies. The study found that mice with inactivated INPP5D gene had more plaques covered by microglia, suggesting unexpected results when modulating inflammation genes.
Researchers found that a gene mutation in mice resulted in increased plaque deposits and larger clumps, suggesting the gene plays a critical role in immune defenses. The study may lead to new therapies targeting this gene mutation to slow progression of Alzheimer's disease.
Researchers at Lund University have discovered that activating the TREM2 receptor on microglial cells slows down Alzheimer's disease progression by clearing tau protein aggregates. This innovative approach may lead to a new treatment method for Alzheimer's disease, in addition to reducing beta-amyloid and tau proteins.
Researchers found that excess fat triggers immune cells to overeat serotonin in the brain of developing male mice, leading to depression-like behavior. Female mice are not affected in the same way, with higher levels of oxytocin linked to social withdrawal.
Researchers found that IGF1 gene therapy increases kisspeptin expression and GnRH release, and alters microglial cell numbers, suggesting a potential protective effect against reproductive decline. This could lead to new strategies for optimizing lifespan and combating age-related health problems in women.
Researchers found drastic differences in microglia marker Iba1 and factors influencing Sirt1 levels and activity between elder groups. Preserving microglia and Sirt1 functional efficiency is crucial for longevity.
Recent studies have shed light on the biological mechanisms that connect sleep and anxiety, highlighting the importance of sleep in regulating stress responses. Research has shown that inadequate sleep can lead to increased anxiety and stress, while also exacerbating mental distress.
Germ-free zebrafish larvae have altered neural connections due to reduced microglia pruning by immune cells. Reintroducing normal microbiota restores normal development and social behavior. Microorganisms stimulate microglial activity, promoting neural connection remodeling.
In a study published in Nature Communications, researchers found that astrocytes take over the role of cleaning up dead microglia, which are normally responsible for this task. This process is crucial for maintaining optimal conditions in the nervous system and preventing accumulation of cellular debris.
Researchers identified a kinase molecule that directs microglia activity, potentially treating neurodegenerative diseases like Alzheimer's and MS. The molecule, called spleen tyrosine kinase, targets plaque buildup and debris accumulation in the brain.
Researchers have discovered that neurons with double-stranded breaks (DSBs) in their DNA actively trigger an inflammatory response, which is mediated by the activation of the NFkappaB transcription factor. This process elicits an immune response from microglia, leading to synaptic loss and cognitive function impairment.
The fasting-mimicking diet reduced Alzheimer's pathology in mice, including amyloid beta and tau protein levels, and showed less brain inflammation. Mice on the diet also performed better on cognitive tests, with some showing improved performance comparable to non-Alzheimer's mice.
Researchers have discovered that two mouse genes, inherited from ancient viral infections, help defend the brain against new bacterial and viral infections. The genes, Rtl5/6, are carried by all mammals and were preserved in the genome for over 120 million years.
Researchers at FIU Stempel College are investigating the translocator protein 18 kDa (TSPO) in relation to Alzheimer's disease. They aim to determine if an increase in TSPO levels is harmful and may be a potential target for treatments.
Researchers discovered specialized direct contact sites between microglial cells and developing neurons, regulating brain development. Inhibiting these interactions disrupts normal cerebral cortex structure, highlighting microglia's crucial regulatory role in brain development.
Scientists developed a laser-based zebrafish model to simulate traumatic brain injuries and identify molecular targets for treatment. The model revealed the importance of microglia activation and brain-derived neurotrophic factor (BDNF) in brain recovery.
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.