Articles tagged with Microglia
Researchers at UCI have developed a mouse model that allows for the study of human brain immune cells in unprecedented detail. The 'chimeric' mouse contains human microglia, enabling the investigation of Alzheimer's mechanisms and potential treatments.
Researchers at Massachusetts General Hospital discovered a key gene interaction that fuels neuroinflammation, leading to cognitive decline and Alzheimer's disease. CD33 and TREM2 genes regulate microglia activity, with CD33 acting as the 'on' switch for inflammation.
The study reveals Galectin-3 plays a key role in regulating immune response associated with Amyloid beta peptide. Researchers have identified genetic mutations linked to increased risk of Alzheimer's, and a potential therapeutic target for blocking galectin-3.
A study has identified a key connection between two damaging proteins in Alzheimer's disease: amyloid beta and tau. Immune cells called microglia may be the missing link between these proteins, which can cause brain tissue damage.
Researchers have developed a microglia-selective fluorogenic probe that triggers fluorescence through gene expression, enabling selective labeling and imaging of microglia cells in live brain tissue. This probe has the potential to detect developing neural diseases such as Alzheimer's disease and stroke.
Researchers found that visual stimulation can prevent neuron degeneration and enhance synaptic function in Alzheimer's disease models. The treatment also improved spatial memory performance in older mice without a predisposition for the disease.
A new study uncovers the presence of 'hidden' microglia in the brain, which show a resemblance to microglia associated with Alzheimer's disease. The researchers hope to find strategies for controlling these immune cells to develop future treatments for neurodegenerative diseases.
Researchers developed a chemical probe that enables live-imaging of microglia in the brain, crucial for understanding brain development and disease. The probe, CDr20, labels microglia in both human- and primate-derived cells, allowing for clinical-relevant studies.
Researchers studied how microglia cells in the brain respond to toxic proteins associated with Alzheimer's disease. The study found that age, sex, and genetics affect microglial response, suggesting that modulating this response could lead to new treatments.
Researchers at Mass Eye and Ear have identified microglia as gatekeepers that orchestrate inflammatory responses in the retina during autoimmune uveitis. By depleting microglia, disease was completely blocked, suggesting a novel therapeutic target for this devastating eye disease.
A new study by University of Notre Dame scientists reveals microglia can cross from the central nervous system (CNS) into the peripheral nervous system (PNS) in response to injury. This finding has broad implications for nervous system diseases and opens up new questions about the function and capabilities of these cells.
A Stanford University School of Medicine study found that blocking a specific protein's activity improved cognitive behavior in aging mice. The researchers identified a gene called CD22, which is involved in microglial phagocytosis and is upregulated with age.
Scientists discovered that microglia, a type of nervous system cell suspected to cause retinal damage, surprisingly had no damaging role during prion disease in mice. Microglia might delay disease progression, providing new insights into inherited photoreceptor degeneration diseases.
Researchers created a high-resolution map of the brain's immune system, showing that all microglia have the same core signature but adapt differently depending on their function. This discovery is significant for understanding brain diseases like multiple sclerosis and Alzheimer's.
A study published in Nature Neuroscience found that individuals with schizophrenia exhibit excessive synaptic pruning, a process normally occurring during adolescence. This abnormality contributes to the development of schizophrenia symptoms.
Researchers at the National Eye Institute discovered that TGF-beta signaling governs immune cell function in the eye, leading to activated microglia and retina damage. Disrupting this signal may represent a potential therapeutic target for treating AMD.
Researchers at Arizona State University discover that choline supplementation may help fight Alzheimer's disease in mice and their offspring. The study reveals that high choline intake during gestation and lactation improves spatial memory in subsequent generations, suggesting a transgenerational effect.
A study published in Nature Neuroscience reveals that defective immune cells in the brain play a key role in Alzheimer's disease. Activating a specific gene, TREM2, can help prevent toxic deposits, but over-activation may have negative consequences.
Research found that activation of microglia in the spinal cord is responsible for increased pain sensitivity in response to stress. Eliminating microglia from the spinal cord prevented these effects, highlighting their role in transmitting pain to the brain.
Researchers at Johns Hopkins Medicine found that the molecular underpinnings of necrotizing enterocolitis (NEC) lead to brain injury. They identified TLR4 as the cause and found that HMGB1 is generated in response to TLR4, leading to microglial activation and brain injury.
Researchers have identified nine distinct groups of microglia, including some that appear only in embryonic or newborn stages, and others that are involved in myelination. These findings may help uncover new roles for microglia in disease and development, and could lead to the development of therapies targeting specific subpopulations.
Researchers at The Ohio State University found that eliminating microglia can reverse some aspects of stress sensitization, but not increased anxiety. Microglia hold unique signatures of chronic stress and play a critical role in the recurrence of anxiety after chronic stress.
Researchers from the Luxembourg Institute of Health uncover distinct microglial signatures in response to acute inflammation, highlighting potential benefits for resolving inflammation. Their single-cell transcriptomic study provides new resources for understanding brain disorders and developing novel therapeutic strategies.
A study in mice found that eliminating microglia cells eliminated inflammation following traumatic brain injury, offering a potential target for treatment. The research aims to understand cellular-level changes associated with sports-related concussion and other brain injuries.
Targeting immune checkpoints in microglia may reduce neuroinflammation in neurodegenerative diseases. Dysregulation of these checkpoints is linked to diseases such as Alzheimer's, Parkinson's, and ALS.
Researchers at Boston Children's Hospital have discovered a 'don't eat me' signal that prevents microglia from pruning useful connections. This 'yin/yang' system helps fine-tune brain circuits, ensuring normal brain development and potentially treating neurodegenerative diseases.
Researchers at MassGeneral Hospital for Children found that microglia play a crucial role in shaping behavior during adolescence, with different effects in males and females. The study suggests that this process could improve understanding of normal behavioral changes and neuropsychiatric disorders that emerge during adolescence.
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.
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.
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.
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.
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 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.
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 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.
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.
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.