Articles tagged with Astrocytes
Scientists at The Wistar Institute have identified a novel mechanism by which astrocytes promote cancer cell growth and metastasis in the brain. The pro-metastatic effect is mediated through the activation of the PPAR-gamma pathway, providing a new lead for PPAR-gamma antagonists in cancer therapy.
Researchers have identified the mechanism underlying ultrasonic brain stimulation's neuromodulation effect, revealing that TRPA1 channels in astrocytes play a crucial role. This non-invasive approach has shown promise for treating movement disorders and may also be useful for conditions like dementia, concussions, and depression.
Researchers at University of Eastern Finland developed a new approach to improve brain drug delivery by utilizing LAT1. The study showed that prodrugs can be converted into active drugs that utilize LAT1 for cell entry, achieving higher concentrations in target cells.
Researchers found that noradrenaline is necessary for astrocytes to respond to local stimulation, effectively integrating sensory and behavioral information. Astrocytes can track distinct information during behavior, including arousal state and sensory experience.
Researchers identified NFIA as a central regulator of reactive astrocytes in brain injury. The study showed that NFIA plays different roles depending on the type of injury and region affected, hinting at an extensive reservoir of reactive astrocyte responses.
A $1.5 million, three-year grant will fund the development of new tools to study astrocytes, key players in brain function and disorders. The tools will allow scientists to manipulate astrocyte properties with spatial and temporal control, enabling investigations into their role in modulating neurons.
Salk scientists discover that astrocytes are required for long-term memory formation and consolidation in mice. The study found that disabling astrocytes led to significant deficits in remote memory retention after a few weeks.
A recent NIH study using a mouse model of stuttering identified the loss of astrocytes as a critical brain cell type involved in the disorder. The research found that this loss was most prominent in the corpus callosum, a part of the brain that bridges the two hemispheres. This discovery could lead to novel interventions for stuttering...
Researchers at Stanford University School of Medicine found a way to improve neuron recovery in rats by blocking a molecule that controls genetic instructions. The approach, if applied to humans, may help patients with stroke, cardiac arrest, or major blood loss recover memory functions.
Researchers have identified a specific role for astrocyte proteins in directing neural connections, using nanoparticles to deliver corrective proteins to replace missing proteins in neurodegenerative diseases. The study offers new hope for regrowing and repairing damaged brain networks.
Researchers identified astrocytic mu-opioid receptors as key to conditioned place preference, a mechanism underlying addictive behaviors. The study found that astrocytic MORs in the hippocampus release glutamates, increasing synaptic transmissions and inducing long-term potentiation, which is responsible for spatial memory acquisition.
Research at Kanazawa University reveals that FGF signaling pathway determines the fate of neural stem cells in cerebral cortex, enabling proper numbers of neurons and astrocytes to be generated. The study sheds light on the mechanisms behind brain disorders caused by unbalanced cell numbers.
Researchers discovered that glia cells, not neurons, calculate when an effort is futile and send a 'quit' message to the body. Glia cells called radial astrocytes amp up their activity when animals stop trying, helping them decide whether to continue or give up.
Research at the Howard Hughes Medical Institute's Janelia Research Campus discovered that astrocytes collect and recycle toxic molecules from overactive neurons, protecting them from damage. This mechanism, previously unknown, could be related to Alzheimer's disease and is an important role for astrocytes beyond their support of neurons.
Researchers at Trinity College Dublin have created a novel brain slice model that captures features observed in patients with mitochondrial epilepsy. The model reveals the critical role of astrocytes in driving seizure generation and demonstrates the involvement of the GABA-glutamate-glutamine cycle.
Researchers at Penn State discovered a simple drug cocktail that converts glial cells into functional new neurons, which can survive for over seven months in a lab culture. The approach has promising implications for treating neurological disorders such as stroke and Alzheimer's disease, with the potential to be used in a pill form.
Scientists have discovered new messenger molecules, miR-494-3p, that regulate genes involved in maintaining neuron health. The study found that introducing this micro-RNA into astrocyte-motor neuron cultures significantly improved neuron survival rates, potentially leading to new therapies for ALS and other neurodegenerative diseases.
Researchers at IUPUI have developed a way to create more-mature models of the human retina using human stem cells and astrocytes. These findings will guide the development of a lab-grown model of glaucoma, enabling researchers to study the disease in greater detail.
Researchers found a correlation between loss of function in patches of astrocytes and development of epilepsy. Altered astrocytes may be the root of epilepsy development after mild traumatic brain injuries.
A new systematic approach has identified environmental factors that boost neurological inflammation, including an herbicide banned in Europe. Researchers found that linuron and another compound increase activity of a gene associated with inflammation.
A study suggests defective astrocytes contribute to α-synuclein accumulation, leading to neuronal degeneration. Researchers discovered that healthy astrocytes can prevent α-synuclein buildup and restore neuronal function when cultured with Parkinson's disease neurons.
A new study reveals that astrocytes can lead the tempo of the body's internal clock and control daily behavior patterns in mammals. The discovery could pave the way for new treatments to manage circadian rhythm disruptions related to health conditions like jet lag, sleep disorders, and dementia.
Researchers found defective astrocytes cause accumulation of toxic alpha-synuclein, leading to neuronal death and degeneration. Healthy astrocytes protect neurons from cell death through restored cellular degradation processes.
Researchers discovered a novel function of nestin in regulating neurogenesis through Notch signaling from astrocytes to neural stem cells. Adult mice deficient in nestin show increased newly born neurons and impaired long-term memory, highlighting the complex role of astrocytes in brain plasticity.
Researchers discovered a two-step control mechanism in neural stem cells that differentiates into neurons and astrocytes. PRC1 represses genes related to neuronal function temporarily and permanently at two distinct stages of brain development.
Scientists have gained a clearer understanding of what happens in the brains of people with Huntington's disease, highlighting the crucial role of glial cells. Glial cell dysfunction is believed to drive neuronal loss and disease progression, leading to motor control problems and cognitive decline.
Researchers have identified a novel mechanism for neuronal regeneration after stroke. By overproducing the protein Slit in neuroblasts, these cells can migrate past activated astrocytes and mature into functional neurons.
A study published in Cell Stem Cell found that glial cell development involves three stages and is regulated by specific transcription factors. The researchers discovered that the proteins NFIA, ATF3, and Runx2 play key roles in organizing glia-specific gene expression.
Astrocytes communicate with neurons to regulate sleep time in fruit flies, a finding that suggests a similar mechanism may exist in mammals. The study used fruit flies to identify mechanisms of sleep regulation and found that a protein called Eiger plays a critical role in regulating sleep.
A NIH study found that astrocytes alter neuron signal speed by changing myelin thickness and node width, impairing reflexes. The researchers propose thrombin inhibitors as a potential treatment for multiple sclerosis.
A study reveals how a single mutation in the GFAP protein, the most common protein in astrocytes, produces devastating effects on brain cells. The mutated protein causes widespread tangles and disturbs cellular processing units, reducing myelin formation.
Astrocytes play an unexpected role in brain plasticity by secreting the protein Chrdl1, which enables the brain's maturation and regulates its flexibility. This discovery could lead to ways to restore lost connections due to aging or trauma.
The study evaluated [18F]SRF101, a PET radiotracer for astrocytosis detection. The results showed no systemic signs of toxicity in mice and estimated the human radiation dosimetry to be comparable to other 18F radiopharmaceuticals.
Researchers at Sanford Burnham Prebys Medical Discovery Institute have identified a previously unknown astrocyte subpopulation that plays a key role in driving brain inflammation. The newly discovered 'ieAstrocytes' are activated early in neuroinflammatory diseases, such as multiple sclerosis and Alzheimer's disease.
Researchers from UCI have identified patterns of sugars on the surface of neural stem cells that determine their fate, affecting brain cell formation. This discovery may improve the use of stem cells in transplantation therapies to treat injury and disease.
A new method allows for rapid generation of functional brain cells, known as astrocytes, from embryonic stem cells in just two weeks. This breakthrough enables researchers to study the role of astrocytes in various diseases, including neurodegenerative conditions such as dementia and ALS.
A team led by W. Christopher Risher discovered that the α2δ-1 receptor is necessary for synapse structure and brain connectivity, implicating astrocyte-to-neuron signaling in psychiatric disorders such as autism and addiction.
A new stem cell model developed by City of Hope researchers provides insight into the disease pathway of Alexander disease, a rare nervous system disorder. The study found that therapies targeting CHI3L1 protein may be able to treat Alexander's disease or leukodystrophic diseases.
A study suggests a simple imbalance in acid-alkaline chemistry inside endosomes may lead to amyloid protein accumulation and nerve cell degeneration. Researchers found that histone deacetylase inhibitors can reverse pH problems and improve amyloid beta clearance in lab-grown mouse brain cells.
Researchers develop experimental drug NLY01 that slows Parkinson's disease progression in mice by blocking degradation of brain cells and protecting nerve cells. The drug, similar to diabetes treatments, may offer a new treatment option for the progressive disorder.
Scientists investigate how high blood pressure affects the balance between blood flow and neuron activity in the brain. High blood pressure can lead to increased calcium levels in astrocytes, which may trigger inflammation and alter protective mechanisms.
A new study found a hitherto unknown error in the transport of glutamine between astrocytes and neurons in mice with Huntington's disease. The researchers believe this area holds potential for developing a future treatment.
Researchers found that overproduction of ephrin-B1 in astrocytes weakens memory retention in mice. In contrast, decreased ephrin-B1 levels lead to more synapses and better learning. The study suggests that glial cells play a crucial role in regulating learning and memory.
Researchers found that APOE4 promotes beta amyloid protein accumulation, leading to Alzheimer's pathology. They also discovered that editing the gene can eliminate signs of Alzheimer's in brain cells.
Researchers have successfully tested an existing prescription drug, fingolimod, on lab cultures infected with mucolipidosis IV (MLIV), a rare genetic disease that causes severe neurological damage. The study suggests that fingolimod may help regulate abnormal astrocyte behavior and improve brain function in MLIV patients.
Researchers aim to enhance neuron protection in glaucoma patients by activating the sigma 1 receptor, potentially increasing long-term protection. The S1R agonists have shown promising results in protecting retinal ganglion cells and may offer a new treatment strategy for glaucoma.
Astrocytes and pericytes work together to regenerate cerebral blood vessels in brain regions damaged by stroke. New blood vessels form at the interface between these cells, re-establishing normal blood flow within weeks.
Researchers at DZNE found that blocking a particular receptor on astrocytes can normalize brain function and improve memory performance in mice models of Alzheimer's. This novel approach holds strong potential for treating the disease by targeting aberrant network dysfunctions in astrocytes.
A deficiency of TRIF, a key innate immune adaptor, significantly shortens the survival time of ALS mice by allowing the accumulation of toxic reactive oxygens. This study reveals a new role for innate immunity in ALS pathomechanism and provides a clue to develop a therapeutic approach for protecting motor neurons.
Researchers at UCLA have developed a new method that enables them to observe astrocytes' influence on nerve-cell communication in real time, shedding light on their role in neurological disorders such as Alzheimer's and Huntington's disease.
Research shows that nanoparticles can cause DNA damage to developing brain cells when exposed to cellular barriers. This damage is dependent on astrocytes and has implications for the development of potential drug targets in treating neurodegenerative conditions.
A new study in mice shows that turning on a gene called LZK can stimulate the healing process after spinal cord injuries, resulting in smaller scars. This trigger has implications for treating brain conditions through gene therapy targeting astrocytes.
Astrocytes may partner with neurons to process information, according to a new MIT study funded by a $1.9 million grant. The research aims to uncover the crucial role of astrocytes in brain function and development, potentially providing insight into disorders such as Alzheimer's disease, schizophrenia, and autism.
Researchers found that silencing astrocytes in the brain's breathing center caused rats to breathe at a lower rate and tire out on a treadmill earlier. Astrocytes were shown to use adenosine triphosphate (ATP) to communicate with other cells, and their modulation was linked to changes in oxygen levels.
Researchers at the Buck Institute for Research on Aging have identified a potential therapeutic avenue for Parkinson's disease by clearing senescent astrocytes, which stop dividing and secrete deleterious factors. This approach shows promise in preventing symptoms of the incurable neurological disorder.
A study in mice suggests that West Nile virus infection can lead to persistent neurological problems due to unresolved inflammation. Targeting this inflammation with an arthritis drug may prevent some of these problems with memory.
Researchers at the Salk Institute discovered that genes that normally sever connections between neurons are reactivated in aging astrocytes, leading to reduced neuronal communication. This may explain age-related cognitive decline and neurological disorders such as Alzheimer's and diabetes.
Gene expression in specific cells and regions provides a more precise, neuroprotective approach than traditional treatments for neurological diseases. Increasing cholesterol synthesis gene expression in astrocytes of the spinal cord can repair nerves affected by walking in multiple sclerosis patients.
Researchers created 3D mini brains using bioengineered 'asteroids' to study neural connections and accelerate disease research. The model allows for rapid screening of drugs and analysis of mutations, paving the way for potential treatments and clinical trials to improve or regenerate impaired nervous systems.
Researchers have developed a new system to study Creutzfeldt-Jakob disease in the laboratory, using brain cells derived from human stem cells. The method enables scientists to infect human cells with prions and replicate the proteins in the lab, providing valuable information for potential treatments.