Researchers developed a gene-delivery system that converts reactive astrocytes into functional neurons, improving motor recovery in mice and rats. The system, TRANsCre-DIONE, selectively targets scar-forming cells and reprograms them into neurons, which generate nerve impulses and receive signals from other neurons.
A new study by UC Berkeley researchers suggests that hyperreactive astrocytes are a primary driver of childhood epilepsy, particularly in the inherited disorder tuberous sclerosis complex. The findings highlight possible therapies to reduce inflammation and alleviate seizures, challenging the traditional view that neurons are the sole ...
Scientists at Salk Institute create first microprotein atlas of human frontal cortex with and without Alzheimer's disease, identifying 1,067 new microproteins and a potential link to immune cell dysfunction in Alzheimer's. The atlas provides a system for investigating microproteins in aging and neurodegeneration, bringing scientists cl...
A new study identifies astrocytes in the brain's fear center as a key player in stress response and anxiety. The research found that restoring the antenna-like structure on these cells can ease stress behaviors, and a potential treatment target has been identified.
Researchers from Fudan University developed a strategy to achieve efficient engraftment of macrophages in peripheral organs using Mr BMT, a technique that replaces microglia in the CNS. The study shows that Mr BMT preserves tissue homeostasis and innate immune response, with durable macrophage replacement lasting at least 9 months.
Two UCLA studies published in Cell and Science uncover the role of metabolism and physical signals in guiding radial glia to produce specific cell types in the developing human cortex. Metabolic research found that the pentose phosphate pathway influences cell fate, while thalamic projections make direct physical contact with radial gl...
Research identifies aberrant ERBB4 expression in excitatory neurons as an early driver of Alzheimer's disease pathologies, including neuronal hyperactivity, synapse loss, and cognitive decline. Manipulating ERBB4 expression in mouse models reveals its role in driving disease features, including reactive gliosis and amyloid buildup.
Salk Institute researchers found microglia's novel way to contribute to ALS progression and death, using TAM receptors to find and kill motor neurons in spinal cords of mice with ALS. The study suggests a new target for therapy innovation, but notes the complexity of variables involved.
Researchers found that female mice's microglia form prolonged contacts with neurons during recovery, leading to synaptic remodeling and plasticity. This phenomenon was not observed in male mice, highlighting differences in brain recovery processes between sexes.
A study found that brain immune cells undergo substantial remodeling in midlife, leading to chronic neuroinflammation and potential dementia risk. The research used advanced single-cell analysis techniques to analyze postmortem hippocampal tissue from 40 healthy adults.
Researchers discovered that reducing microglial activity worsened abnormal electrical activity and increased seizure-like events in a mouse model of Alzheimer's disease. Microglia are not just drivers of inflammation but also perform important housekeeping functions to maintain healthy brain activity.
Researchers found that KCL-286 enhances DNA repair and reduces neuronal inflammation in a mouse model of Alzheimer's disease. The drug activates the retinoic acid receptor-beta pathway, promoting the expression of certain repair genes.
Researchers developed a human-safe drug that repairs DNA breaks and reduces inflammation in a mouse model of Alzheimer's disease. The approach targets multiple disease-relevant cellular pathways, providing a broader therapeutic strategy than previous approaches focused on individual disease hallmarks.
Scientists at King's College London have developed a human-safe drug that repairs DNA breaks and reduces inflammation in a mouse model of Alzheimer's disease. This approach targets multiple features of the disease simultaneously, providing a broader therapeutic strategy than previous approaches focused on individual disease hallmarks.
Researchers discovered astrocytes actively preserve long-term memories by regulating Ank2 and BDNF signaling. This finding expands the understanding of how memories are stored in the brain.
Researchers have identified an experimental molecule called OLE that can restore part of the brain's protective function against Alzheimer's disease. The compound helps microglia enclose and contain beta-amyloid plaques, reducing their size and toxicity.
Researchers have identified an experimental molecule called OLE that helps restore microglia's protective function against Alzheimer's disease. The compound reduces beta-amyloid plaque size and toxicity, improving cognitive performance in memory tests.
Researchers analyzed brain tissue from MSA patients and found that the immune cells known as microglia appear to be exhausted or dysfunctional in later stages of the disease. The study suggests that an overactive immune system may contribute to the development of MSA, providing a potential target for future treatment.
Researchers uncover role of glia in ALS pathogenesis, finding altered functioning of TDP-43 protein and MYC factor responsible for abnormality. The study provides new anchors to understand clinical heterogeneity of ALS and suggests potential biomarkers for diagnosis and monitoring.
Researchers discovered that strokes cause a chain reaction within the brain, leading to neuronal cell death. They found that blocking collagen production can prevent this damage and even restore motor function in paralyzed monkeys. The new drug KDS12025 reduces hydrogen peroxide levels and prevents the entire process from being triggered.
Researchers from the Salk Institute found that astrocytes play a crucial role in fragile X syndrome symptoms. Correcting dysregulations in star-shaped brain cells improved some symptoms, including reduced seizures and restored molecular balances in a mouse model of FXS. The study validates the importance of studying astrocytes in FXS r...
Researchers develop molecular tool called SynTrogo, which enables selective dismantling of synaptic connections in brain circuits. By harnessing astrocytes, the system reduces synapse number while strengthening remaining connections, leading to enhanced long-term potentiation and improved memory.
Recent discoveries have shed light on gene expression control in tumor growth, revealing the critical role of epigenetic marks and genomic imprinting. The findings have significant implications for cancer treatment, as they suggest that disrupting the tumor's access to neural signaling may halt its growth.
A new study reveals that astrocytes regulate inhibitory signaling in the cerebellum during development, enabling the emergence of flexible and precise motor coordination. In contrast, younger animals rely on neuron-derived tonic inhibition, which is replaced by astrocyte-derived tonic inhibition in late adolescence.
A new study reveals that astrocytes actively participate in motor-learning circuit rewiring by eliminating synapses in the striatum. The research identifies MEGF10 as a key molecular mediator of this process, which is regulated by dopamine signaling and neural activity.
Cancer cells tap into the nervous system's power grid by forming synaptic contacts with nerve cells, promoting tumor growth and spread. Venkataramani's research aims to repurpose the drug perampanel for glioblastoma treatment and develop gene therapy approaches to disconnect tumors from the nervous system.
Scientists found that blocking microglia prevents infant forgetting and improves memory in mice, suggesting a role for microglia in memory formation. Microglia inhibition also enhances engram cell activation, providing a functional explanation for enhanced memory recall.
Research highlights glial cells as dynamic regulators of brain health, playing both protective and harmful roles in neural function. Promising therapeutic targets include oligodendrocyte dysfunction, mitochondrial transfer, and extracellular vesicle engineering.
Scientists at Lund University have created a new method to directly reprogram glial cells into parvalbumin neurons, which can help regulate brain activity and potentially treat disorders such as schizophrenia and epilepsy. The breakthrough could lead to therapies that replace lost or damaged brain cells in the future.
Researchers discovered that female brain immune cells called microglia express more interferon-related genes when responding to amyloid-β plaques, causing more harm to neuronal connections. This finding suggests a potential sex-specific treatment approach for Alzheimer's disease.
Scientists at Salk Institute find protein CCN1, secreted by astrocytes, maintains stable neural circuits in adult brains. The discovery could lead to new therapeutics for brain injury and stroke.
Astrocytic glutamine synthetase plays a key role in regulating glutamate signaling, contributing to nicotine-induced brain changes and locomotor sensitization. A custom-designed peptide inhibits this process, demonstrating the importance of astrocyte communication in nicotine addiction.
Researchers have identified a new immune process that clears toxic amyloid plaques and delays cognitive decline in Alzheimer's disease. The 'Fc fragment' of the monoclonal antibody Lecanemab activates microglia, the brain's immune cells, to remove plaques more efficiently.
Researchers found that a protein involved in ATP release, connexin 43, plays a key role in depressive- and anxiety-like behaviors. Restoring connexin 43 in the hippocampus improved behavioral outcomes and boosted ATP levels in stressed mice.
Researchers identify a rare gene mutation that appears to protect the brain's immune cells from damage caused by Alzheimer's disease. The study reveals how this mutation can confer resilience on the brain, potentially leading to new therapeutic approaches.
A new study reveals that astrocytes, a type of glial cell, are responsible for stabilizing memories through repeated engagement. The researchers found that Fos activity in astrocytes only occurs during recall, and that these cells can be activated to produce stable memories.
Research reveals that ovarian aging is not just about egg quality, but also the surrounding cells and tissues. The study found that eggs cluster in pockets surrounded by egg-free zones, which decline in density with age, influencing egg lifespan and maturation.
Researchers found that an astrocytic 'brake' mechanism, fueled by the neurotransmitter GABA, blocks spinal cord repair after injury. Inhibiting this pathway with the MAOB inhibitor KDS2010 enables recovery of spinal cord function in animal models.
A USF-led Nature study identifies how a genetic variant disrupts microglia function, increasing Alzheimer's disease risk. The PICALM gene defect impairs waste-processing organelles in microglia, causing harmful lipid droplets to accumulate and weaken their ability to clear debris.
Research reveals neuroglia play active role in brain function, driving disease progression through atrophy and functional decline. Therapeutic strategies targeting neuroglial signaling may prevent damage following brain injury or protect against neurodegenerative processes.
Researchers have discovered that microglia, the brain's immune cells, play a key role in how the brain adapts during adolescence. This understanding may transform how neurodevelopmental disorders are treated during this window and possibly into adulthood. The study also found that microglial contact with axons increases dopaminergic ci...
Researchers have reimagined hemoglobin as an antioxidant protein in the brain, where it breaks down harmful reactive oxygen species. A new compound, KDS12025, selectively enhances this natural defense mechanism to protect against ALS, Parkinson's, Alzheimer's, and autoimmune disorders.
Researchers at the Institute for Basic Science have discovered that excessive GABA produced by astrocytes impairs fear extinction in PTSD. A new brain-permeable drug called KDS2010 has reversed PTSD-like symptoms in mice, providing a promising therapeutic approach.
Laminin-411 protein and its derived peptide A4G47 exhibit pro-myelinating activity in oligodendrocytes, promoting myelin sheath formation. This discovery advances understanding of myelin sheath formation and potential applications for treating demyelinating diseases.
In a breakthrough study, researchers at the University of Rochester Medical Center found that microglia cells respond differently than neutrophils to photoreceptor damage in the retina. This discovery has high implications for treating vision loss caused by photoreceptor cell damage.
Researchers discovered a two-step mechanism where inhibitory neurons release nitric oxide to rapidly dilate blood vessels, followed by slower, localized vasodilation via astrocyte activation. This breakthrough sheds light on how neural signals are translated into blood volume changes in brain imaging.
A combination of two approved cancer medications may slow or reverse Alzheimer's symptoms by reversing gene expression changes in neurons and brain cells. Researchers analyzed public data from deceased donors and found a link between these drugs and reduced risk of developing the disease.
A recent study using machine learning and computational modeling reveals that astrocytes play a more active role in brain function than previously thought. Astrocytes subtly modulate communication between neurons during synchronous brain activity, influencing network coordination and stability.
Researchers at Florida Atlantic University have secured two key grants to investigate targeting the MBLAC1 gene as a new approach to treat glioblastoma, a very aggressive and fast-growing type of brain cancer. The project aims to advance innovative projects that could make a meaningful impact on cancer therapy.
A UC Riverside study found that Toxoplasma gondii can significantly disrupt brain function by interfering with communication between brain cells. Infected neurons release fewer extracellular vesicles, which can lead to seizures, neural damage, or altered brain connectivity.
Astrocytes, once thought to be supporting cells, are active players in neuromodulation, controlling neuronal activity and behavior. The discovery of a biochemical circuit involving ATP and adenosine reveals a slower time scale for modulation compared to neural circuits.
Researchers found that astrocytes transmit signals, revealing new ways the brain processes information. The study provides direct evidence for the real-time action of astrocytes in live brains of fruit flies, suggesting their role in mediating neurophysiology and behavior.
Researchers at Linköping University developed a miniaturized iontronic micropipette to precisely modulate neuronal and astrocytic activity. The study revealed dynamic dynamics between cells, highlighting the importance of chemical signaling in brain function.
Researchers have found that promoting glucose metabolism in glial cells can relieve inflammation and photoreceptor degeneration in Alzheimer's patients. This discovery presents an exciting new therapeutic target for treating neurodegenerative conditions like Parkinson's.
A USC Stem Cell mouse study has identified shared genes involved in regenerating cells in the ear and eye, which could lead to new treatments for hearing and vision loss. The researchers discovered that inhibiting a specific protein, p27Kip1, can encourage regeneration in both organs.
A review article reveals CD2AP's crucial role in amyloid metabolism, tau pathology, synaptic function, and neuroinflammation in Alzheimer's disease. CD2AP deficiency accelerates plaque formation, while its loss in neurons leads to reduced spine density and impaired synaptic plasticity.
Studies have consistently shown that 40Hz gamma stimulation can improve cognitive function and reduce Alzheimer's pathology in mice. In human clinical trials, participants exposed to 40Hz light and sound experienced significant slowing of brain atrophy and improvements on some cognitive measures compared to untreated controls.
Researchers at Johannes Gutenberg University Mainz have discovered that histone deacetylase 8 (HDCA8) inhibits the conversion of Schwann cells into their repair phenotype, slowing down peripheral nervous system recovery. Removing HDAC8 accelerates regeneration and restores sensory function.
A fungal infection has been shown to trigger a fruit fly's own immune system to destroy brain cells leading to signs of neurodegeneration. The fungus makes the fly's innate immune system release Sarm, which suppresses the immune response and kills brain cells.
Researchers found that glial cells accumulate excess extracellular matrix proteins and alter gene expression when detecting damaged cilia. This discovery may have implications for treating diseases caused by defective cilia, such as polycystic kidney disease.