Articles tagged with Astrocytes
Research found that astrocytes from children with autism exhibit innate inflammation, contributing to neuronal dysfunction. However, when normal astrocytes were co-cultured with autistic neurons, the latter reverted to normal functioning.
Salk Institute scientists discovered that astrocytes induce communication between pairs of neurons early in development through glypican 4. The protein increases receptors on postsynaptic neurons, enabling active connections. This breakthrough offers a promising therapeutic target for neurological disorders.
Scientists at the Salk Institute have identified a key protein complex involved in regulating brain cell identity, with high levels of Nup153 found to be necessary for maintaining precursor status. This finding may provide new insights into the underlying causes of neurological disorders such as schizophrenia and Alzheimer's disease.
A study by Valeria Valente identified genetic alterations promoting aggressiveness in astrocytomas, with correlations to patient survival prognosis. The research aimed to customize treatment to patient needs, potentially predicting tumor behavior through gene signatures.
A new study published in Neuron confirms that lab-grown astrocytes mature at the same rate as human brains, providing a valuable technique to investigate their role in brain development and disease. The findings have significant implications for understanding the roots of neurological disorders such as schizophrenia and autism.
New study finds that human brain cells from individuals with childhood-onset schizophrenia disrupt communication in mice, exhibiting anti-social and anxious behaviors. The researchers suggest that glial cell dysfunction is a primary contributor to the disease.
Researchers at Salk Institute developed a new protocol to derive astrocytes from human stem cells, which could provide breakthroughs for treatments of stroke, Alzheimer's and psychiatric disorders. The method allows for faster and more effective production of astrocytes, enabling researchers to model neurological disorders in a dish.
Scientists have discovered how certain forms of motor neuron disease begin and progress, revealing potential new ways to slow down or even stop the process. Healthy astrocyte-supporting cells may play a role in combating neurodegenerative diseases.
A new study reveals that blood vessels in the brainstem constrict when oxygen levels rise, unlike other parts of the body. This specialized response helps maintain proper breathing and is made possible by astrocytes releasing signaling molecules.
Neuroscientists at Tufts University have discovered a new signaling pathway that connects two major receptors in the brain associated with learning and memory. Astrocytes play a key role in regulating this pathway by sensing wakefulness and releasing chemicals that activate these receptors.
Researchers at Medical College of Georgia are exploring the potential of (+)-pentazocine to prevent vision damage in glaucoma patients by activating sigma-1 receptors in astrocytes. The study aims to understand how increased pressure affects astrocyte behavior and develop new therapies to protect neurons.
The study reveals that CD38 is essential for postnatal glial cell development, particularly astrocytes. The gene's absence leads to retardation of glial cell development and aberrant interactions among cells, resulting in developmental disorders.
A study at Massachusetts General Hospital found that two major types of brain tumors, astrocytomas and oligodendrogliomas, may originate from the same type of neural progenitor cells. The analysis revealed differences in gene mutation patterns and tumor microenvironments between the two subtypes.
Researchers found that phototherapy improved behavioral responses and recovered myelin sheaths in rat models of diabetic neuropathy. The treatment also reduced the migration of astrocytes to the site of injury, which release inflammatory mediators.
Researchers at Washington University in St. Louis have discovered that astroglia, or astrocytes, help set the pace of the suprachiasmatic nuclei to schedule a mouse's day. Altering astrocyte clocks slowed mice's sense of time, highlighting their influence on daily behavior and physiological processes.
A research team at Brigham and Women's Hospital has revealed how FTY720 suppresses chronic inflammation in the central nervous system to reduce pathogenic activities of astrocytes. The findings suggest this treatment may hold promise for progressive and difficult-to-treat forms of multiple sclerosis.
Research at Baylor College of Medicine and Texas Children's Hospital found that specific brain cell subpopulations play a role in epilepsy. Astrocytes were divided into distinct subpopulations, each with unique gene expressions and functions. These subpopulations may contribute to brain tumor progression and seizure onset.
Astrocytes have long been linked to neurodegenerative diseases, but their roles were unknown. New research reveals that injured or diseased astrocytes can be toxic to neurons, causing cell death. However, they also play a crucial role in regeneration and connection formation.
A Stanford-led study found that astrocytes, once thought to be supporting cells, can become toxic and destroy nerve cells, driving many neurodegenerative diseases. The discovery has profound implications for treating these diseases by blocking or countering the toxin secreted by harmful astrocytes.
Researchers found that glial cells experience bigger changes than neurons as people age, with astrocytes and oligodendrocytes shifting their regional gene expression patterns upon aging. The study provides a tool to understand how aging in the brain may be linked to the causes of age-related disorders.
Researchers at DZNE discovered that astrocytes potentiate harmful electrical discharges after a stroke, leading to increased brain damage. Modulating astrocyte calcium metabolism may be a potential starting point for treating stroke in humans.
Astrocytes play a crucial role in brain tissue recovery after injury, with the Ror2 protein promoting their proliferation. The research team discovered that Ror2 is activated by basic fibroblast growth factor, which enables astrocytes to start proliferating and minimizing inflammation around damaged neurons.
A study published in Cell Reports reveals that astroglial cells play a crucial role in forming the corpus callosum, a bridge-like structure connecting the two hemispheres of the brain. Without this cellular support, callosal agenesis occurs, affecting 1 in 4,000 people and leading to developmental disorders.
Researchers found that glial cells, including astrocytes, are impaired by the genetic defect and involved in symptoms of fragile X syndrome. The study suggests looking beyond neuronal effects to fully understand the disease.
Researchers at TUM discovered that brain cells, specifically astrocytes, regulate sugar intake and adjust metabolism in response to hormones like insulin and leptin. This paradigm shift could lead to new treatments for diabetes and obesity by targeting multiple cell types involved in metabolic processes.
Astrocyte calcium signaling properties studied in visual cortex to understand their role in brain function and potential involvement in multiple brain disorders. The study aims to shed light on fundamental properties of astrocytes, providing a baseline for comparing and testing their role in brain disorders.
A new study suggests that a long version of waxy ceramide, often found in skin creams and shampoos, plays a critical role in supporting brain cells called astrocytes. The researchers aim to understand how this lipid regulates cilia on brain cells and prevent neurodegeneration associated with Alzheimer's disease.
Researchers at Tufts University School of Medicine identified a novel astroglia-mediated pathogenic mechanism contributing to fragile X syndrome symptoms. The study found that disrupting an astrocyte-specific glutamate transporter contributed to FXS-like symptoms, which were reversed by restoring FMRP and glutamate signaling.
Researchers found that the LRP4 molecule is crucial for regulating glutamate levels in star-shaped brain cells called astrocytes. Without it, glutamate release is reduced, leading to intellectual impairment and seizures. However, blocking the receptor ATP eventually activates ameliorates the negative impact on mice.
UC Riverside researchers found that Toxoplasma infection disrupts neurotransmitters in the brain, leading to neurological disease in predisposed individuals. Treatment with ceftriaxone restored GLT-1 expression, reducing extracellular glutamate and normalizing neuronal function.
By transplanting healthy human glia cells into mice with Huntington's disease, researchers were able to reduce symptoms and slow disease progression. The transplanted cells restored normal neuronal activity and rescued nerve cells at risk of death.
Researchers at SISSA have developed a gene therapy approach targeting glioblastomas by introducing an active version of the Emx2 gene, which inhibits astrocyte growth and leads to tumour cell suicide. The treatment has demonstrated efficacy in both vitro and in vivo tests, with potential for preventing aggressive recurrence development.
A study by University of Bonn researchers identifies hippocampal astrocytes as key regulators of memory processing, prioritizing new information over stored memories. The discovery sheds light on the cellular causes of dementia and Alzheimer's disease.
Biologists at the University of Iowa have identified a group of genes, gamma-protocadherins, that regulate dendrite growth in neurons. These genes must be an exact match for each neuron to correctly grow dendrites.
Researchers at RIKEN Brain Science Institute have demonstrated that astrocytes regulate changes in synaptic strength, which is crucial for learning and memory. By examining cultured cells and brain slices, they found that astrocyte activity helps maintain normal variation of synaptic strengths.
The University of Houston has received a $386,000 grant from the Robert J. Kleberg Jr. and Helen C. Kleberg Foundation to develop a model for studying traumatic brain injuries (TBI). Professor Amy Sater aims to create a system that can screen for possible drugs facilitating recovery from brain injury using Xenopus laevis tadpoles.
A study published in The Journal of Clinical Investigation identified a key role for S1 astrocytes in sustaining mechanical allodynia. Researchers found that specific signaling pathways activated in the brain contribute to neuropathic pain, suggesting new therapeutic targets.
A recent mouse study reveals that scar-forming cells called astrocytes are required for repair and regrowth following spinal cord injury. The research supports axon growth through astrocyte scars, challenging the long-held idea that scars hinder neuronal regrowth.
Researchers found that transcranial direct current stimulation causes synchronized calcium surges from astrocytes, reducing depressive symptoms and increasing neural plasticity. This effect is absent when blocking astrocytic calcium surges, highlighting their importance in therapeutic outcomes.
Loss of major histocompatibility complex I (MHCI) expression in motor neurons leads to vulnerability to ALS astrocyte toxicity. Studies show that increased MHCI expression is protective against astrocyte-induced death, providing a potential translational target for ALS treatment.
Montreal scientists have discovered a mechanism that enables brain cells to adjust their support for neurons, potentially improving brain function or restoring lost potential in disease. The discovery sheds light on the complex functioning of astrocytes, star-shaped cells that protect and support brain neurons.
UTSA associate professor Carlos Paladini receives a $1.8 million grant to investigate dopamine bursts and astrocytes in the brain, with potential applications for treating clinical depression, drug addiction, schizophrenia, and Parkinson's disease.
A trio of molecules, hevin, neurexins, and neuroligins, orchestrate neuron connections in the developing brain that are responsible for processing sensory information. The study may provide insight into brain disorders including autism, depression, and addiction.
Scientists at Augusta University found that YAP helps control astrocyte function, regulating the protective blood-brain barrier. Without YAP, astrocytes become hyper-reactive, leading to deadly inflammation and potential hydrocephalus.
Human astrocytes have unique genes and respond differently to neurotransmitters, particularly glutamate, suggesting improved detection of neuroactivity. The study's novel method allows researchers to compare astrocytes from healthy tissue and those affected by diseases such as glioblastoma and epilepsy.
Researchers discovered that astrocytes are repelled by amyloid plaques, contrary to previous assumptions. This finding suggests that modifying astrocyte function rather than changing position may be a key response to plaque formation.
A fruit fly model of Alexander disease has been developed to study astrocyte dysfunction and its role in neurodegeneration. Nitric oxide has been identified as a critical mediator in the process.
Researchers from the University of Zurich have confirmed the existence of a concentration gradient of lactate between astrocytes and neurons in the intact mouse brain. The study provides new evidence for an exchange of lactate between different brain cells, supporting a 20-year-old hypothesis on brain energy metabolism.
Researchers discovered that antidepressant amitriptyline increases FGF2 mRNA expression in astrocytes through RTK activation. This signaling cascade could guide the development of novel antidepressants with new mechanisms. The study expands on previous findings, identifying EGR1 as a necessary protein for FGF2 expression.
Researchers at Massachusetts General Hospital found that urate stimulates astrocytes to activate an antioxidant pathway believed to have a role in several neurodegenerative disorders. A phase 3 trial of a urate-elevating drug, led by Dr. Michael Schwarzschild, is planned to enroll 270 patients with early-stage Parkinson's disease.
Researchers found that treating astrocyte nucleus with TGF-beta frees p75NTR protein, allowing critical molecules to enter the nucleus and enabling reactive state. This discovery highlights the importance of nuclear pore complex in brain health and raises possibilities for treating neurological disorders.
A UBC study suggests targeting healthy cells around tumors to stop brain cancer from spreading. The research team found that glioma cells can hijack astrocytes, regulating their environment to stimulate tumor growth and invasion.
A research group at Hiroshima University found that downregulated spinal astrocyte connexin43 expression leads to sustained neuropathic pain following peripheral nerve injury. Restoring Cx43 function via adenovirus vector may reverse mechanical hypersensitivity and modulate glutamatergic neurotransmission.
Scientists have established a model for latent HIV infection of brain cells and identified various compounds that can affect latency. The study aims to develop new therapeutic approaches to silence the virus in brain cells, which could improve clinical care for HIV-1 patients.
Astrocytes play a crucial role in maintaining healthy vascular tone by releasing signals to dilate or constrict blood vessels as needed. This basal control helps regulate blood flow and prevent damage from excessive pressure or calcium levels.
A new study by Naguib Mechawar's team found that networks of astrocytes are altered specifically in areas of the brain associated with mood regulation. The research also discovered unique properties of astrocytes in subcortical brain regions, which may contribute to depression and suicide.
Researchers at the University of Montreal have discovered that astrocytes control the pattern of neuronal electrical activity, determining functions such as chewing, locomotion, and respiration. The study reveals a mechanism by which astrocytes regulate calcium levels, leading to changes in neural function.
Aromatase, an enzyme converting testosterone to estrogen, plays a significant role in the healthy and injured brain. In healthy brains, it helps neurons produce estrogen, maintaining cognitive function. After injury, aromatase expression shifts to astrocytes, aiding their support of stressed neurons and promoting recovery.
Researchers at University of Queensland discovered a molecule called C5aR exacerbates inflammation and tissue damage after spinal cord injury. Administering an experimental drug that inhibits C5aR can improve recovery when given early after injury, potentially treating patients with spinal cord trauma.
Researchers at the University of Bonn have discovered a new cause of temporal lobe epilepsy: astrocyte uncoupling. This leads to hyperexcitability of neurons and epileptic seizures. The study suggests that inflammation plays a role in uncoupling astrocytes, which can be reversed at an early stage.