Articles tagged with Microglia
Researchers have discovered axonal dysregulation in the prenatal brain as a mediator of genetic risk for schizophrenia. The study used induced pluripotent stem cells and three-dimensional brain organoids to identify key genes involved, including CYFIP1, which is highly expressed in microglia.
Researchers at Kyushu University have successfully converted brain immune cells into neurons, which restored brain function after a stroke-like injury in mice. The findings suggest that replenishing neurons from immune cells could be a promising avenue for treating stroke in humans.
Researchers have discovered new insights into microglia-astrocyte communication and its impact on intracerebral hemorrhage, as well as the testicular toxicity of triptolide. Additionally, a study on epicardial cells has identified key gene markers associated with cardiac regenerative therapy strategies.
A recent study published in Nature Medicine suggests that complement proteins and microglia can be activated early in the development of Huntington's Disease, leading to synapse loss and cognitive decline. By blocking these proteins, researchers were able to prevent or slow cognitive defects and motor symptoms in animal models.
Scientists at Temple University's Alzheimer's Center have identified a promising new therapeutic target for Alzheimer's disease: the protein ABCA7. The study found that cholesterol depletion and inflammation suppress ABCA7 levels in human brain cells, potentially contributing to disease onset.
Researchers identify somatostatin-positive interneurons as crucial in maintaining cognitive function, and their dysfunction leads to impaired memory and learning. The study uses a toxin to ablate these cells, resulting in mice exhibiting cognitive deficits similar to those seen in aging humans.
Researchers analyzed over 2 million cells from 400 postmortem brain samples to identify cellular pathways that could become new drug targets for Alzheimer's treatments. They found impairments in mitochondrial function, synaptic signaling, and protein complexes, as well as disrupted lipid metabolism.
A recent study by Ohio State University researchers found that saturated fats can interfere with the creation of new memories in aged brains. However, omega-3 fatty acids, particularly DHA, may help protect brain cells from fat-related inflammation. The study used cell cultures and brain tissue from aging mice to explore the effects of...
An international team has decoded the TSPO protein to visualize neuroinflammation, revealing its relationship with microglial cells. The study's findings pave the way for optimizing observation of neuroinflammatory processes and re-reading previous studies.
Scientists have identified thousands of non-coding genetic variants linked to Alzheimer's disease, focusing on their impact on microglial gene expression and function. The study found that turning off specific regions can affect multiple genes, highlighting the complex mechanisms underlying AD.
Microglial cells age differently in male and female mice, with female microglia displaying a 'middle-aged' phenotype and male microglia switching suddenly to an aged phenotype. The researchers identified key genes and mechanisms contributing to this aging process, including the role of aged-like microglia in cognitive decline.
The collaboration has garnered $5.68 million of grant support, with a five-year $2.13 million National Institutes of Health R01 grant and a five-year $2.89 million NIH R01 grant. Researchers are using computational biology to model a key Alzheimer's protein called TREM2 and its interactions with small chemical molecules.
Researchers at St. Jude Children's Research Hospital discovered a subset of immune cells that slows Alzheimer's disease progression by interacting with microglia. The cells, called CD8+ T cells, use a molecular handshake to signal to the microglia to stop causing uncontrolled inflammation, which in turn slows plaque growth and symptoms.
Researchers found that ferroptosis, a form of cell death caused by iron buildup, destroys microglia cells in the brain's immune response, contributing to cognitive decline. The study's findings may lead to the development of compounds targeting microglial degeneration, offering new hope for Alzheimer's and vascular dementia treatments.
Researchers have identified a new cell type, ARG1+ microglia, involved in brain development and function during early postnatal stages. This discovery sheds light on the role of microglia in neural systems and their potential link to neurodevelopmental and neurodegenerative diseases such as Alzheimer's.
A new molecule called A11 has been found to reduce inflammation and improve memory in models of Alzheimer's disease. By targeting the genetic transcription factor PU.1, A11 suppresses inflammatory gene expression in microglia immune cells, leading to reduced neurodegeneration and improved cognition.
Researchers have successfully transplanted human microglia cells into mouse retina, creating a model for studying treatments for diabetic retinopathy, glaucoma, and age-related macular degeneration. The study demonstrates the potential of microglial replacement therapy to treat retinal and central nervous system diseases.
Researchers find immunotherapy treatment anti-CTLA-4 leads to greater survival in mice with glioblastoma and discover new way cells kill cancer by triggering microglia, specialized immune cells in the brain. This breakthrough could lead to more effective treatments for human brain cancer.
A study found that border-associated macrophages play a crucial role in neuroinflammation and neurodegeneration in Parkinson's disease. Deleting MHCII from these cells reduced neuroinflammation, suggesting they are essential for presenting alpha-synuclein antigens to T cells.
Researchers found that Alzheimer's patients exhibit heightened sensitivity to light changes, which can contribute to 'sundowning' and disease progression. Light therapy could help manage these symptoms and potentially slow disease progression.
Research in rats suggests that loss of immune cells late in gestation may factor into the onset of maternal behavior. Depletion of microglia, a type of immune cell, sped up care for rat newborns in non-mom female rats.
A study by Forsyth Institute researchers reveals a link between periodontal disease and amyloid plaque formation in the brain. Oral bacteria can travel to the brain, causing neuroinflammation and promoting cognitive decline in Alzheimer's patients.
Researchers have found that microglial cells in the brain can serve as a stable viral reservoir for latent HIV. This discovery provides new insights into how to target and eradicate the virus, particularly in the brain or peripheral blood.
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.
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.
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.
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.
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 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.
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.