Articles tagged with Axons
Researchers created stunning images of branching patterns of individual sensory nerve cells, defining ten distinct groups that likely correspond to differences in what the nerves do. The branching patterns can help scientists make sense of known responses to stimulation of the skin and may hold clues for pain management.
Researchers at Johns Hopkins Medicine discovered that a specific protein helps nerve cells extend themselves along the spinal cord during mammalian development. The protein, dystroglycan, acts as a hub for instructional molecules that guide nerve axons as they grow.
IRC researchers led by Dr. Frédéric Charron have made a significant discovery about the internal clock of nerve cells during embryonic development, which could lead to new tools for repairing and regenerating damaged nerve cells in the central nervous system.
A gene called spastin plays a critical role in axon regeneration, which was found to be shut down by a mutation in the gene. The researchers used fruit flies as a model organism and observed that severed axons regrew normally when the gene was present.
Researchers discovered a new mechanism by which STAT3 helps prevent axon degeneration, a hallmark of neurodegenerative diseases. CNTF treatment stimulated STAT3 to inhibit stathmin, leading to increased axon growth and reduced breakdown in ALS patients.
Scientists at Max Planck Institute for Medical Research in Heidelberg have developed a method to prepare the whole mouse brain for
Neural stem cells successfully regenerates axons across the site of complete spinal transaction, leading to functional recovery in rats. The study also showed that adult cells can regenerate into neural stem cells, establishing a new relay circuit that can be measured electrically.
Scientists at Drexel University have found that a key protein involved in nerve cell repair is produced locally in the axons, triggering a molecular distress signal. This discovery may help better understand and control the repair process to speed up recovery from nerve injuries.
Researchers discovered that importin beta1, a crucial protein for nerve repair, is produced locally in the axons of peripheral nerve cells. This finding has significant implications for treating nerve damage and may lead to better treatments and faster repair.
Researchers at KAIST used triangular shapes to guide axon growth in a dish, finding that smaller vertices were more effective in inducing growth. The study aims to develop a reproducible neural circuit model for learning and memory studies as well as drug screening applications.
Researchers at WashU Medicine identified a protein called dual leucine zipper kinase (DLK) that regulates signals telling the nerve cell it's injured, allowing nerve regeneration. The study shows DLK governs whether the neuron turns on its regenerative program.
Researchers at UMass Chan Medical School have identified the first gene, dSarm/Sarm1, responsible for promoting axon destruction after injury. The discovery provides a new therapeutic target to delay or stop axon decay in neurodegenerative diseases.
A team of researchers at Baylor College of Medicine has identified a distal axonal cytoskeleton as the boundary that ensures AnkyrinG clusters properly. The findings suggest that AnkyrinG cannot move beyond this boundary, resulting in proper formation of the axon initial segment and subsequent neural function.
Researchers discovered a large number of unique mRNAs in dendrites and axons, which may be involved in synaptic plasticity and memory formation. The findings suggest that local protein synthesis plays a crucial role in maintaining and modifying the synaptic protein population.
Researchers at Max Planck Institute of Experimental Medicine discovered that glial cells pass on metabolites to neurons, enabling them to generate energy. The study found that oligodendrocytes can replenish energy in nerve fibers through glycolysis, reducing oxidative stress and cell damage.
A study is underway to document the consequences of low-dose exposure to organophosphates, a common pesticide that can impact nerves and cause chronic disabilities such as learning and memory problems. The researchers aim to identify ways to mitigate the effects of these chemicals on brain function.
Researchers at Penn have identified a critical role of Nmnat in maintaining healthy nerves and protecting against degeneration. The enzyme helps stabilize mitochondria, which are essential for nerve cell health.
A study published in PNAS refutes the long-held hypothesis that organelle transport deficits cause axon degeneration in ALS. Instead, reduction and initiation appear to occur through different mechanisms, making axonal organelle transport an unsuitable therapeutic target.
MDC researchers have identified a crucial function of the c-Maf gene in the development of neurons responsible for mechanosensory function. In mice with deleted c-Maf, high-frequency vibrations are not detected, leading to impaired touch sensation and early-onset cataracts.
Scientists have developed a new procedure to rapidly induce nerve regeneration, restoring partial function within days and full function within two to four weeks. The approach mimics the cellular mechanism used by invertebrates to repair damaged nerve axons.
Scientists discovered a gene mutation causing hereditary spastic paraplegia, which may provide clues to axon degeneration in conditions like multiple sclerosis. The study highlights new disease mechanisms that could lead to genetic counselling and testing for affected families.
A study at Boston Children's Hospital found that autism spectrum disorders may involve disordered white matter in the brain, with patients exhibiting higher radial diffusivity values and disorganized axon pathways compared to healthy controls.
A $1.4 million NIH grant will investigate a method to heal peripheral nerve damage by stimulating the growth of Schwann cells and axons, potentially restoring function in patients with severe injuries. Researchers aim to develop effective tools for nerve repair using electrical stimulation technologies.
Scientists at Boston Children's Hospital discover that motor nerve fibers can regrow but not communicate with muscle fibers in time. A limited time window exists for nerve regeneration and functional reactivation, highlighting the need for prompt treatment.
Researchers discovered a molecular mechanism allowing signals from target cells to support neuron survival. Activated protein Rac plays a crucial role in long-range signaling and retrograde transport of neuronal survival signals.
Researchers at Ohio State University have developed a cell-culture system that mimics the coating of nerve cells with protective myelin, opening up new possibilities for studying multiple sclerosis. The study found that myelin regulates key protein placement and activity in sending electrical signals along hippocampal axons.
Case Western Reserve University researchers developed a new computer modeling method that accurately predicts how peripheral nerve axons respond to electrical stimuli, slashing the process from weeks to just seconds.
Researchers at the Institut de recherches cliniques de Montréal (IRCM) have made a breakthrough in understanding how neurons connect and communicate. Drs. Artur Kania and Tzu-Jen Kao discovered that axon guidance is modulated by ligands present within the same neuron, leading to increased diversity of neuronal connections.
Researchers at Institut de recherches cliniques de Montréal have identified a key molecule directing axons during neural circuit formation. VEGF plays a crucial role in attracting nervous system axons, offering potential for therapies to re-grow axons after spinal cord injuries.
A new study suggests that disrupting the supply chain of nerve cells may contribute to Parkinson's disease. Researchers found that a drug called MPP+ damages mitochondria, which can't be transported to axons, leading to cell death.
A study led by Subhojit Roy reveals how certain proteins in neurons travel at a slower pace than others, assembling into larger complexes that move down the axon. The proposed model suggests a 'plume' of proteins, where complexes disassemble and reassemble as they progress, making the overall motion slow and coordinated.
Scientists have discovered a previously unknown type of axonal degeneration called focal axonal degeneration (FAD), which is responsible for damage to nerve cells in multiple sclerosis. FAD can be reversed if recognized and treated early, suggesting a potential target for therapeutic intervention.
Researchers at Northwestern University have made a groundbreaking discovery in the field of neuroscience, finding that axons can transmit signals to the cell body and even communicate with each other. This challenges conventional wisdom on how neurons operate, revealing a new layer of complexity in neural communication.
Scientists have discovered a genetic partnership between two proteins that enables nerve cells to connect correctly in the brain. The study suggests that similar mechanisms may play a role in human brain development and could lead to new therapies for developmental disorders.
Researchers have identified a key molecular mechanism in nerve fibers that ensures rapid conductance of nervous system impulses. The myelin sheath, which acts as an insulating membrane, allows electrical impulses to hop from one node to the next along the axon.
A new Scripps Research study has mapped the dynamic changes in brain connectivity during development, revealing that connections are constantly forming and dissolving. The research highlights the importance of understanding these mechanisms to better comprehend conditions such as autism and schizophrenia.
Brain cells need to create links early on in their existence to ensure successful connections across the brain. This is demonstrated through computer analysis of nerve cell connectivity patterns in roundworms, showing that most neurons develop long-distance connections by being physically close together.
Researchers found a previously unknown link between two ion channels that can cause symptoms in MS patients. The sodium and leak current channels play a crucial role in signal transmission, and manipulating their balance may lead to new therapeutic opportunities.
A disease mechanism linking hereditary amyotrophic lateral sclerosis (ALS) to the more common sporadic form has been discovered. The findings point to the P38 enzyme as a key factor in disrupting axonal transport, a disruption that results in loss of connectivity and symptoms of ALS long before the neurons actually die.
A team of scientists has created a brain atlas that maps the connections between different parts of the human brain. This atlas will help researchers better understand disorders such as autism and schizophrenia, which are believed to be caused by abnormal connections among different regions within the brain.
Researchers at UCI have found a new diagnostic tool for multiple sclerosis by detecting increased levels of antibodies that inhibit energy production in neurons. This breakthrough could lead to earlier and more effective treatment for the chronic disease.
Researchers at the University of California, San Diego School of Medicine found that removing three key inhibitory molecules from myelin did not significantly improve axon regeneration in damaged spinal cords. The study suggests that successful regeneration will require a combination of many approaches and techniques.
Scientists at Queensland Brain Institute have discovered an alternative mechanism for growth cone steering, which could lead to better understanding of nervous system development and cognitive disorders. The discovery has potential implications for research into Parkinson's disease and autism.
Researchers at Babraham Institute identify Nmnat2 as a key axon survival factor that delays degeneration when injured. Boosting Nmnat2 levels may delay degeneration in neurodegenerative diseases like Motor Neurone Disease and Multiple Sclerosis.
Researchers at Boston Children's Hospital found that mutations in TSC2 cause improper axon guidance, leading to abnormal brain connectivity. The study suggests that autism may involve sensory overload or lack of filtering of information.
A new study published in Neuron suggests that deleting a suppressor of inflammatory signaling in mice promotes vigorous axon regeneration after injury. The research also identifies a key growth factor involved in the process and provides potential therapeutic targets.
A study published in Neuron found that deleting a gene called SOCS3 allows mouse axons to regenerate vigorously after injury. The research suggests that the mTOR pathway and JAK/STAT signaling pathway can be manipulated to promote axon regeneration, potentially leading to improved recovery from brain or spinal cord injuries.
Researchers have discovered that fruit fly neurons can rebuild themselves after injury, with a structurally and functionally different component replacing the damaged part. The study reveals a dynamic microtubule response, where dendrites convert to axons, offering potential avenues for understanding axon regeneration.
Scientists at the University of California, San Diego School of Medicine report that regeneration of central nervous system axons can be achieved in rats even when treatment is delayed by more than a year after the original spinal cord injury. The team used a combination of treatments to coax chronically injured axons to regenerate and...
Researchers at MDC Berlin-Buch have identified a protein, CNP, that triggers the splitting of sensory axon growth cones. This discovery sheds light on neuronal branching and its role in transmitting sensations such as touch, pain, and temperature.
Researchers have found that neurons integrate synaptic inputs locally before sending signals to the central axon, similar to how electoral votes contribute to a president's election. The study suggests a two-stage model of dendritic integration, which could lead to better understanding of brain processes like learning and memory.
Researchers successfully guided regenerating sensory axons to their correct targets and formed synapses, but not electrically active connections due to lack of myelin sheath. The study suggests that restoring the myelin sheath is crucial for fully restoring function in injured spinal cords.
Tiny membrane-bound compartments called vesicles rely on axon tension to dump neurotransmitters into the synapse. The researchers found that axons need tension to keep vesicles clustered near the synapse, essential for neuronal signaling. Further research is needed to understand the exact mechanism behind this process.
Researchers have identified a crucial molecular pathway required for the formation of brain neural circuits. This breakthrough has significant implications for understanding how axons reach their targets, paving the way for new therapies to treat spinal cord injuries, neurodevelopmental disorders, and neurodegenerative diseases.
Researchers discovered a sorting mechanism that filters proteins into dendrites and axons, enabling finer control over neurons. The study's findings may enable more precise targeting of neurological disorders and basic research applications.
Scientists at UC San Diego School of Medicine have clearly shown regeneration of critical nerve fibers required for voluntary movement. The breakthrough uses genetically engineered neurons to over-express receptors for BDNF, enabling corticospinal axon regeneration.
Researchers at University of Pennsylvania School of Medicine have engineered transplantable living nerve tissue that encourages and guides regeneration in an animal model. The lab-grown nerves successfully promoted nerve regeneration after injury by acting as a 'living scaffold' for host axons to regenerate across the damage site.
A Stanford study found that stimulating neural wires rather than cells in the subthalamic nucleus can improve Parkinson's symptoms, offering new insights into the disease and possible treatments. The researchers used optogenetics to activate specific types of cells in rodents, revealing a key role for axons in transmitting signals.
Researchers found that blocking dual leucine zipper kinase (DLK) gene may help prevent degeneration of ailing nerve cell branches, a potential trigger for painful neuropathy. The study could lead to the development of a drug to spare cancer patients considerable pain during chemotherapy.
Researchers found that two receptors, neogenin and Unc5B, work together to guide a growing axon towards its destination. The discovery sheds light on how the axon navigates through the body and could have implications for understanding neurological disorders.