Articles tagged with Microglia
A new study from the University of Illinois found that dietary fiber can reduce brain inflammation in old mice, leading to improved memory and reduced cognitive decline. The researchers discovered that high-fiber diets elevated butyrate levels in the blood, which had anti-inflammatory properties on microglia.
Research reveals obesity activates microglia, consuming healthy synapses and leading to dendritic spine loss. Microglial activity is causally linked to obesity-induced cognitive decline, suggesting a potential therapeutic target for this condition.
Researchers found that ACE inhibitors can block the activation of brain cells called microglia, which contribute to memory loss and cognitive impairments in SLE patients. The study suggests that these drugs may be used to preserve the memory of lupus patients.
Researchers at Max Delbrück Center for Molecular Medicine found significant differences in male and female mice microglia structure and function. Male microglia are more active and respond differently to injury, but may also be less protected against environmental insults.
Chronic inflammation caused by failed sensor mechanism can lead to brain cells' loss in old age. The study suggests that CB1 receptors on neurons control microglial cell activity.
Researchers discovered that brain microglia clearance activity in different regions goes hand in hand with natural neuronal degeneration. Microglia can mistakenly attack healthy neurons if their 'eating' behavior is turned on inappropriately, leading to cellular changes associated with neurodegenerative diseases.
Researchers identified a molecular key, P2X4 receptor, that delays Multiple Sclerosis (MS) progression by reducing chronic inflammation and promoting repair responses in the nervous tissue. The study found that activating this receptor improves symptoms during the disease's chronic phase.
Microglia, specialized immune cells in the brain, have been found to gobble up the remnants of injured neurons, preventing damage from spreading to neighboring neurons. This discovery could lead to new strategies for boosting microglial clearance and limiting neurodegeneration after brain or spinal cord injury.
Immune cells called microglia are precision cleaning machines protecting the central nervous system from damage. By understanding their role, scientists can develop new treatments tailored to individual patients' needs.
Researchers at Mass Eye and Ear found that microglial cells rapidly migrate into the injured retina, forming close connections with infiltrating immune cells and removing injured photoreceptors. This protective role of microglia may suggest a new therapeutic avenue for preserving photoreceptors after retinal detachment.
Researchers discovered that microglia can defend against prion infections by trapping and destroying aggregated prion proteins. Eliminating microglia with a specific drug accelerated disease progression in infected mice. The findings suggest targeting microglia to slow the course of prion diseases, including Alzheimer's and Parkinson's.
A study published in Nature sheds light on the connection between the gut and brain, revealing a new pathway that may help guide therapies for multiple sclerosis and other neurologic diseases. Researchers found that compounds produced by gut microbes can limit inflammation in the brain through their influence on microglia.
Researchers at Karolinska Institutet have created a new disease model for neurodegenerative diseases like ALS and MS using the TGF-β protein. This model shows that monocytes can transform into microglia-like cells in response to TGF-β, which could lead to the development of new immunotherapies for these devastating diseases.
Researchers found that microglia's immune response to inflammation can create a 'memory' that worsens Alzheimer's and stroke. The study suggests that environmental factors could trigger long-term changes in the brain's immune cells, leading to increased disease severity.
Scientists at University of Virginia Health System have found evidence that doctors can load custom blends of immune cells into the brain to battle diseases like Alzheimer's. The discovery enables doctors to tailor immune responses without radiation, a major breakthrough in treating neurological disorders.
Researchers captured microglia nibbling on brain synapses for the first time, showing they help synapses grow and rearrange. The findings suggest that microglia may actually strengthen synapses rather than weaken them.
Researchers discovered that a common Parkinson's gene mutation alters immune cells' reaction to generic infections like colds, triggering an inflammatory reaction in the brain. This 'second hit' initiates the destruction of brain areas responsible for movement.
Researchers found that microglia in the retina can repopulate themselves and re-establish their normal organization and function after being nearly eliminated. The discovery could lead to new therapies for controlling inflammation and slowing progression of rare retinal diseases.
Research published in Frontiers in Molecular Neuroscience found that a combination of caloric restriction and low-fat diet prevents activation of brain's immune cells, called microglia, in aging mice. Exercise was significantly less effective than caloric restriction in preventing these changes.
Researchers successfully deciphered the origin of repopulated microglia in the brain and retina, revealing that they are solely derived from residual microglia after acute depletion. This study provides insights for regenerative medicine and sheds new light on the origins and maintenance of microglia in the retina.
Researchers at University of Pennsylvania School of Medicine found that microglia, a type of brain immune cell, are essential for dealing with TDP-43-associated neuron death in ALS. Microglia proliferation and activation helped clear accumulated human TDP-43 from motor neurons, restoring muscle function and mobility.
Researchers developed a new model of HIV infection in microglia using CRISPR/Cas9 gene editing technology, which will aid in understanding how the virus damages the brain and developing anti-HIV therapies. The model also offers a means to evaluate therapeutic strategies targeting the virus in challenging host cells.
Researchers discovered that Zika virus is transmitted from mother to fetus by infected microglia cells, which later develop into the brain's defense system. The finding suggests a potential therapeutic target for reducing Zika transmission and offers hope for preventing devastating neurological damage.
Researchers found that high-risk TREM2 variants can hobble the immune system's ability to protect against amyloid beta, but later in the disease, the absence of TREM2 protein protects the brain from damage. The study suggests targeting the TREM2 protein as a means of preventing or treating Alzheimer's may be complicated and that doctor...
A new study published in Brain Behavior and Immunity appears to challenge the theory that microglia play a role in fetal alcohol spectrum disorders (FASD). The research found no difference in microglial activity between mice exposed to alcohol early in development and healthy animals.
Researchers at King's College London have identified a gene, DLG4, associated with brain damage caused by pre-term birth. The study found that DLG4 is involved in controlling the inflammatory process and may open doors for effective treatments of diseases such as cerebral palsy and autism.
Researchers have discovered that stabilizing TREM2, a protein involved in neurodegenerative diseases, could be a viable therapeutic strategy to combat Alzheimer's disease. The study found that a mutation in the TREM2 gene accelerates its cleavage, leading to reduced full-length protein on microglia cells.
A new study reveals significant differences in the genes expressed by human and mouse microglia, with unique human genes playing a crucial role in immune response. The findings provide valuable insights for studying neurodegenerative diseases such as Alzheimer's and Parkinson's.
A study of 85,000 subjects identified three new gene variants that contribute to the development of Alzheimer's disease by affecting the brain's immune cells. Researchers believe these findings offer fresh ideas for targeting the immune system to fight the disorder.
Researchers at Johns Hopkins Medicine discovered that controlling the immune system's cell reactivity to injury can accelerate eye tissue regeneration in zebrafish. This finding may lead to new strategies for combating degenerative eye diseases in humans.
Researchers have identified altered ANK1 gene expression in microglia cells of individuals with Alzheimer's disease, which is associated with neuroinflammation. The study found that increased ANK1 expression in microglia may be a response to neurodegeneration and neuroinflammation.
A recent study published in Cell Metabolism found that brain-resident immune cells called microglia play a crucial role in driving overeating and weight gain in mice fed high-fat diets. The study suggests that targeting microglia could provide a novel approach to treating obesity, potentially avoiding side effects of existing medications.
Research suggests that dysfunctional microglia cells can induce neurodegeneration in Alzheimer's by increasing phagocytosis of β-amyloid peptides, leading to synapse loss. This study provides new insights into the role of microglia cells in neurodegenerative diseases.
Complement component C3 is produced by microglia in the brain within days of viral infection, suggesting a localized immune response. This finding adds to understanding of how increased expression of immunologic factors contributes to neuroinflammation and seizures following viral infection.
A new study reveals that microglial cells are essential for normal brain function, and impaired TREM2 gene expression can lead to devastating consequences. The researchers found that mutations in the TREM2 gene disrupt microglial function, leading to impaired phagocytosis and catastrophic effects on energy metabolism.
Microglia, the brain's front line of immune defense, have been characterized for the first time. Genes linked to neurological diseases are highly expressed in microglia, suggesting a link between the cells and neurodegenerative and psychiatric illnesses.
Scientists have developed a high-throughput protocol to derive human microglia from stem cells, which can be used to investigate the role of microglia in neurological disorders. This new method enables researchers to generate microglia from individual patients' samples and advance complex disease modeling in a dish.
Mutations in progranulin protein result in obsessive-like behaviors and immune system alterations, implicating TNF as a potential therapeutic target for FTD. Targeting NF-B activity in microglia may also prevent excessive grooming and improve social behavior.
Researchers at UCI have developed a method to generate human microglia cells from skin stem cells, providing a powerful new approach to study and potentially treat neurological diseases like Alzheimer's. This discovery marks an important step in using induced pluripotent stem (iPS) cells for targeted approaches.
A new study suggests that brain inflammation and cognitive decline following surgery are triggered by the brain's own microglia. In a mouse model, experimental oral drug depletion of microglia ahead of surgery prevented memory loss and reduced inflammatory molecules in the hippocampus.
A recent study by Georgia State University researchers found that female brains have more active immune cells in pain processing regions. This leads to improved response to opioid pain medication, often less effective in females.
A new study from Drexel University College of Medicine suggests that a commonly used antibiotic, minocycline, may exacerbate cognitive deficits in newborn rats with traumatic brain injury. The researchers hypothesize that the treatment, which targets inflammation, may be ineffective or even harmful to developing brains.
A recent study published in Cell Reports reveals that microglia turnover is 10 times faster than previously thought, allowing for multiple renewal cycles throughout a person's life. This groundbreaking finding has significant implications for understanding the role of microglia in neurodegenerative diseases like Alzheimer's.
A new tissue culture system has revealed that microglia from aged brains are engulfing amyloid plaques on site, with young microglia secreting factors to rejuvenate older cells. The discovery highlights a potential strategy for removing amyloid plaques and improving cognition in Alzheimer's disease.
Microglia coordinates reinforcements to warn neighbouring cells of invading virus, recruiting astroglia and neurons to remove injured or killed cells. The discovery aims to contribute to new treatment of brain diseases like multiple sclerosis and Alzheimer's disease.
Researchers found higher distribution volume in 8 brain regions among NFL players compared to nonplayers, suggesting localized brain injury may be associated with football play. Limited white matter changes were observed in the brains of NFL players.
Researchers discovered that glioblastoma cells inhibit caspase-3 activity in microglia, leading to a tumor-stimulating phenotype. This inhibition causes microglia to stimulate tumor cells instead of attacking them.
Researchers at National Institute for Physiological Sciences have discovered that microglia, immune cells in the brain, directly contact neurons to form new connections and strengthen brain connectivity. This finding could deepen understanding of developmental disorders such as autism and schizophrenia.
Research published in Frontiers in Cellular Neuroscience found that seasonal allergies can lead to increased neuron production in the hippocampus, a region responsible for forming new memories. This discovery raises questions about the long-term consequences of allergies on brain development and function.
Researchers discovered that microglia brain immune cells play a major role in the initiation and maintenance of neuropathic pain. Targeting these cells within a few days after nerve injury can greatly reduce chronic pain in animals. This breakthrough could lead to more effective painkillers with fewer side effects.
Researchers found that long-term antibiotic treatment decreased levels of amyloid plaques and activated inflammatory microglial cells in mice brains, while altering the gut microbiome. The study suggests a link between the gut microbiome's composition and immune system activity impacting Alzheimer's disease progression.
Researchers have identified a link between the TREM2 gene and immune cell dysfunction in Alzheimer's disease. Studies found that variants of this gene can impair the brain's ability to clear amyloid-beta aggregates, a hallmark of the disease.
A recent study by McGill University Health Centre researchers found that microglia can reduce the adverse changes to neural circuitry caused by chronic cocaine use. Microglia may be enticed to keep going by stimulating their production of TNF, which suppresses synaptic changes caused by cocaine.
Salk scientists discovered that specific immune receptors in the brain play a crucial role in clearing both healthy and dying neurons. In their absence, new neurons increased dramatically in certain regions, suggesting that these receptors may also target living but dysfunctional cells.
A new study reveals that a targeted immune pathway may be the key to preserving cognitive function in Alzheimer's disease. By blocking this pathway, researchers were able to reduce synapse loss in mouse models of the disease, offering hope for a potential therapeutic target to halt its progression.
A new study reveals that immune cells called microglia play a crucial role in rewiring brain connections, a process essential for neuroplasticity and learning. By 'pruning' unwanted connections, microglia enable the formation of new pathways between neurons.
Researchers have identified a new biomarker associated with the activation of an innate immune response to neural damage during early stages of Alzheimer's disease. The concentration of a specific segment of the protein TREM2 in cerebrospinal fluid is significantly elevated in early stages of the disease.
A new biomarker of brain inflammation in early-stage Alzheimer's disease has been identified, indicating that microglia-mediated inflammation may demarcate the transition from preclinical to full dementia. The TREM2 protein fragment in cerebrospinal fluid levels closely mirror microglia activity during the course of the disease.
Researchers found that flushing away inflammatory cells contributed to restored memory function in test mice with Alzheimer's disease. The study suggests targeting these cells with specific drugs may be a promising new approach.
Researchers identify microglia cells as primary cause of cognitive problems in MS patients, disrupting communication between nerve cells. The findings suggest that the disease's impact on cognition is more complex than previously thought, with potential new targets for treatment.