Articles tagged with Astrocytes
Astrocyte senescence is linked to excitotoxicity in cortical neurons involved in memory, highlighting aging as a major risk factor for neurodegeneration. The study identifies targets for drug development to slow pathology.
A recent study published in Scientific Reports reveals that Zika virus infection causes damage to astrocytes, leading to oxidative stress, DNA breakage, and permanent mutations. This damage can contribute to brain malformations like microcephaly and potentially other neurological disorders.
Astrocytes support memory function through distinct molecular pathways triggered by norepinephrine release. Norepinephrine promotes synaptic plasticity and energy metabolism for memory consolidation.
Researchers reveal a key role for astrocytes in facilitating inhibitory neuron growth into the lateral geniculate nucleus during early brain development. Without retinal inputs, astrocyte function is disrupted, leading to the absence of inhibitory interneurons.
A new study suggests that targeting astrocyte calcium signaling could decrease amphetamine behavioral effects and potentially develop therapies for diseases with dysregulated dopamine. Astrocytes were previously considered 'support cells', but now shown to actively contribute to brain function.
Increasing 40Hz gamma rhythm power in the brain has been shown to strengthen neural connections and improve symptoms in Alzheimer's disease models. The study used light flickering or sound buzzing at 40Hz to achieve this effect, which was found to decline pathological amyloid and tau protein buildups and protect neurons from degeneration.
A new pathway in the central nervous system removes brain waste substances through the creation of corpora amylacea (CA), aggregates formed by glucose polymers. CA acts as waste substance containers that are expelled from the nervous system and removed by the immune system.
Researchers used human induced pluripotent stem cells and CRISPR/Cas9 gene editing to model chemical changes in GFAP protein associated with Alexander disease. The study reveals differences in GFAP modifications depending on symptom onset time, allowing for new drug development opportunities.
Researchers have made significant progress in understanding brain function by studying the role of lactate in memory formation and learning. The study, published in Progress in Neurobiology, used a novel technique to produce three-dimensional models of astrocytes, revealing their complex structure and metabolic coupling with neurons.
Researchers at Georgetown University Medical Center found that exposure to polychlorinated biphenyls (PCBs) impairs brain function in mice by activating pathways that neutralize toxins and causing oxidative stress in astrocytes. This study suggests a potential contributing factor to neurodegenerative disorders.
A study led by UCLA researchers found that suppressing the mutation in astrocytes can stop the progression of Huntington's disease in mice and repair some of the damage. The findings suggest that impaired astrocytes play a role in many neurological diseases, including Alzheimer's and ALS.
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 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.
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.
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.
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.
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 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 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.
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.
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 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.
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.
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.